Publications by authors named "Junjie Xiao"

165 Publications

Protocol of a Prospective Cohort Study of Physical Activity in Cardiovascular Outcomes (PACVO) in China: Objective, Design, and Baseline Characteristics.

J Cardiovasc Transl Res 2022 Jan 8. Epub 2022 Jan 8.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong, 226011, China.

Physical inactivity has been known as an independent risk factor for cardiovascular diseases (CVDs). The "Physical Activity in Cardiovascular Outcomes (PACVO)" study is a long-term community-based cohort study, which will prospectively observe the association of physical activity alone or combined with other contributor factors with CVD outcomes. From 2013 to 2014, a total of 8291 participants ≥ 18 years old were enrolled in the PACVO study from Jidong community (Tangshan, China). According to physical activity assessment, participants were divided into inactive, moderately active, and very active groups. The follow-up has been conducted once every year including physical examinations, blood biochemistry, cardiovascular imaging, and life quality questionnaires until 2034 or until the occurrence of cardiovascular events. The PACVO study will provide substantial information about the association of physical activity with CVD outcomes, therefore promote utilizing physical activity in the prevention and prediction of CVDs.
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http://dx.doi.org/10.1007/s12265-021-10194-wDOI Listing
January 2022

Hallmarks of exercised heart.

J Mol Cell Cardiol 2021 Dec 14;164:126-135. Epub 2021 Dec 14.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong 226011, China; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Life Science, Shanghai University, Shanghai 200444, China. Electronic address:

The benefits of exercise in humans on the heart have been well recognized for many years. Long-term endurance exercise training can induce physiologic cardiac hypertrophy with normal or enhanced heart function, and provide protective benefits in preventing heart failure. The heart-specific responses that occur during exercise are complex and highly variable. This review mainly focuses on the current understanding of the structural and functional cardiac adaptations to exercise as well as molecular pathways and signaling proteins responsible for these changes. Here, we summarize eight tentative hallmarks that represent common denominators of the exercised heart. These hallmarks are: cardiomyocyte growth, cardiomyocyte fate reprogramming, angiogenesis and lymphangiogenesis, mitochondrial remodeling, epigenetic alteration, enhanced endothelial function, quiescent cardiac fibroblast, and improved cardiac metabolism. A major challenge is to explore the underlying molecular mechanisms for cardio-protective effects of exercise, and to identify therapeutic targets for heart diseases.
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http://dx.doi.org/10.1016/j.yjmcc.2021.12.004DOI Listing
December 2021

Exercise downregulates HIPK2 and HIPK2 inhibition protects against myocardial infarction.

EBioMedicine 2021 Dec 24;74:103713. Epub 2021 Nov 24.

Shanghai Engineering Research Center of Organ Repair, Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong 226011, China; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai, 200444, China. Electronic address:

Background: Exercise can protect myocardial infarction (MI) and downregulate cardiac Homeodomain-Interacting Protein Kinase 2 (HIPK2). However, the role of HIPK2 in MI is unclear.

Methods: HIPK2 mice and miR-222 rats, HIPK2 inhibitor (PKI1H) and adeno-associated virus serotype 9 (AAV9) carrying miR-222 were applied in the study. Animals were subjected to running, swimming, acute MI or post-MI remodeling. HIPK2 inhibition and P53 activator were used in neonatal rat cardiomyocytes (NRCMs) and human embryonic stem cell-derived cardiomyocytes (hESC-CMs) subjected to oxygen glucose deprivation/reperfusion (OGD/R). Serum miR-222 levels were analyzed in healthy people and MI patients that were survival or readmitted to the hospital and/or died.

Findings: Cardiac HIPK2 protein levels were reduced by exercise while increased in MI. In vitro, HIPK2 suppression by lentiviral vectors or inhibitor prevented apoptosis induced by OGD/R in NRCMs and hESC-CMs. HIPK2 inhibitor-treated mice and HIPK2 mice reduced infarct size after acute MI, and preserved cardiac function in MI remodeling. Mechanistically, protective effect against apoptosis by HIPK2 suppression was reversed by P53 activators. Furthermore, increasing levels of miR-222, targeting HIPK2, protected post-MI cardiac dysfunction, whereas cardiac dysfunction post-MI was aggravated in miR-222 rats. Moreover, serum miR-222 levels were significantly reduced in MI patients, as well as in MI patients that were readmitted to the hospital and/or died compared to those not.

Interpretation: Exercise-induced HIPK2 suppression attenuates cardiomyocytes apoptosis and protects MI by decreasing P-P53. Inhibition of HIPK2 represents a potential novel therapeutic intervention for MI.

Funding: This work was supported by the grants from National Key Research and Development Project (2018YFE0113500 to JJ Xiao), National Natural Science Foundation of China (82020108002, 81722008, and 81911540486 to JJ Xiao, 81400647 to MJ Xu, 81800265 to YJ Liang), Innovation Program of Shanghai Municipal Education Commission (2017-01-07-00-09-E00042 to JJ Xiao), the grant from Science and Technology Commission of Shanghai Municipality (18410722200 and 17010500100 to JJ Xiao), the "Dawn" Program of Shanghai Education Commission (19SG34 to JJ Xiao), Shanghai Sailing Program (21YF1413200 to QL Zhou). JS is supported by Horizon2020 ERC-2016-COG EVICARE (725229).
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http://dx.doi.org/10.1016/j.ebiom.2021.103713DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8626841PMC
December 2021

Exercise and cardiovascular protection: Update and future.

J Sport Health Sci 2021 Dec 16;10(6):607-608. Epub 2021 Nov 16.

Cardiovascular Research Center, Division of Cardiology, Corrigan Minehan Heart Center, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address:

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http://dx.doi.org/10.1016/j.jshs.2021.11.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8724613PMC
December 2021

Non-coding RNA basis of muscle atrophy.

Mol Ther Nucleic Acids 2021 Dec 19;26:1066-1078. Epub 2021 Oct 19.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong 226011, China.

Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), play vital roles in muscle atrophy. This review mainly discusses the regulation of ncRNAs in muscle atrophy induced by various factors such as heart failure, cancer cachexia, aging, chronic obstructive pulmonary disease (COPD), peripheral nerve injury (PNI), chronic kidney disease (CKD), unhealthy habits, and usage of hormones; highlights the findings of ncRNAs as common regulators in multiple types of muscle atrophy; and summarizes current therapies and underlying mechanisms for muscle atrophy. This review will deepen the understanding of skeletal muscle biology and provide new strategies and insights into gene therapy for muscle atrophy.
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http://dx.doi.org/10.1016/j.omtn.2021.10.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8569427PMC
December 2021

Physical Exercise Protects Against Endothelial Dysfunction in Cardiovascular and Metabolic Diseases.

J Cardiovasc Transl Res 2021 Sep 17. Epub 2021 Sep 17.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong, 226011, China.

Increasing evidence shows that endothelial cells play critical roles in maintaining vascular homeostasis, regulating vascular tone, inhibiting inflammatory response, suppressing lipid leakage, and preventing thrombosis. The damage or injury of endothelial cells induced by physical, chemical, and biological risk factors is a leading contributor to the development of mortal cardiovascular and cerebrovascular diseases. However, the underlying mechanism of endothelial injury remains to be elucidated. Notably, no drugs effectively targeting and mending injured vascular endothelial cells have been approved for clinical practice. There is an urgent need to understand pathways important for repairing injured vasculature that can be targeted with novel therapies. Exercise training-induced protection to endothelial injury has been well documented in clinical trials, and the underlying mechanism has been explored in animal models. This review mainly summarizes the protective effects of exercise on vascular endothelium and the recently identified potential therapeutic targets for endothelial dysfunction.
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http://dx.doi.org/10.1007/s12265-021-10171-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8447895PMC
September 2021

Percutaneous Intracoronary Delivery of Plasma Extracellular Vesicles Protects the Myocardium Against Ischemia-Reperfusion Injury in Canis.

Hypertension 2021 11 7;78(5):1541-1554. Epub 2021 Sep 7.

Cardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University, The Sixth People's Hospital of Nantong (H.W., Y.X., C.S., M.W., J.Z., J.X., J.X.), Shanghai University, China.

[Figure: see text].
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.121.17574DOI Listing
November 2021

Animal exercise studies in cardiovascular research: Current knowledge and optimal design-A position paper of the Committee on Cardiac Rehabilitation, Chinese Medical Doctors' Association.

J Sport Health Sci 2021 Dec 25;10(6):660-674. Epub 2021 Aug 25.

Institute of Geriatrics, Affiliated Nantong Hospital of Shanghai University, Sixth People's Hospital of Nantong, School of Medicine, Shanghai University, Nantong 226011, China; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, School of Life Science, Shanghai University, Shanghai 200444, China. Electronic address:

Growing evidence has demonstrated exercise as an effective way to promote cardiovascular health and protect against cardiovascular diseases However, the underlying mechanisms of the beneficial effects of exercise have yet to be elucidated. Animal exercise studies are widely used to investigate the key mechanisms of exercise-induced cardiovascular protection. However, standardized procedures and well-established evaluation indicators for animal exercise models are needed to guide researchers in carrying out effective, high-quality animal studies using exercise to prevent and treat cardiovascular diseases. In our review, we present the commonly used animal exercise models in cardiovascular research and propose a set of standard procedures for exercise training, emphasizing the appropriate measurements and analysis in these chronic exercise models. We also provide recommendations for optimal design of animal exercise studies in cardiovascular research, including the choice of exercise models, control of exercise protocols, exercise at different stages of disease, and other considerations, such as age, sex, and genetic background. We hope that this position paper will promote basic research on exercise-induced cardiovascular protection and pave the way for successful translation of exercise studies from bench to bedside in the prevention and treatment of cardiovascular diseases.
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http://dx.doi.org/10.1016/j.jshs.2021.08.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8724626PMC
December 2021

Sex bias in alcohol research: A 20-year comparative study.

Front Neuroendocrinol 2021 10 16;63:100939. Epub 2021 Aug 16.

Clinical Medical Research Institute and Department of Metabolic and Bariatric Surgery, First Affiliated Hospital of Jinan University, Guangzhou, China. Electronic address:

We aimed to assess the sex-inclusive and sex-based analysis bias in alcohol research for the past 20 years. Data were abstracted from 2988 original research articles published from 2000 through 2019 in 51 representative journals across 9 biomedical disciplines. An analysis in 5-year intervals revealed that the percentage of studies using participants of both sexes was significantly higher between 2015 and 2019 than between 2000 and 2014. When stratified, clinical studies showed a higher percentage of both-sex studies compared to basic studies using animals. The reasons for the use of single-sex cohorts mainly included insufficient participant numbers and misconceptions surrounding the hormonal variability of females. Implementation of the NIH SABV policy promoted the ratio of NIH-funded papers with sex-based analyses. In conclusion, sex bias in alcohol-related biomedical studies has improved over the past 20 years, particularly after the implementation of the SABV policy. Although clinical studies increasingly included sex-based analysis, basic studies were biased towards the use of males.
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http://dx.doi.org/10.1016/j.yfrne.2021.100939DOI Listing
October 2021

ADAR2 increases in exercised heart and protects against myocardial infarction and doxorubicin-induced cardiotoxicity.

Mol Ther 2022 Jan 16;30(1):400-414. Epub 2021 Jul 16.

Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai 200444, China; Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China. Electronic address:

Exercise training benefits the heart. The knowledge of post-transcription regulation, especially RNA editing, in hearts remain rare. ADAR2 is an enzyme that edits adenosine to inosine nucleotides in double-stranded RNA, and RNA editing is associated with many human diseases. We found that ADAR2 was upregulated in hearts during exercise training. AAV9-mediated cardiac-specific ADAR2 overexpression attenuated acute myocardial infarction (AMI), MI remodeling, and doxorubicin (DOX)-induced cardiotoxicity. In vitro, overexpression of ADAR2 inhibited DOX-induced cardiomyocyte (CM) apoptosis. but it could also induce neonatal rat CM proliferation. Mechanistically, ADAR2 could regulate the abundance of mature miR-34a in CMs. Regulations of miR-34a or its target genes (Sirt1, Cyclin D1, and Bcl2) could affect the pro-proliferation and anti-apoptosis effects of ADAR2 on CMs. These data demonstrated that exercise-induced ADAR2 protects the heart from MI and DOX-induced cardiotoxicity. Our work suggests that ADAR2 overexpression or a post-transcriptional associated RNA editing via ADAR2 may be a promising therapeutic strategy for heart diseases.
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http://dx.doi.org/10.1016/j.ymthe.2021.07.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8753375PMC
January 2022

Erratum: Crucial Role of miR-433 in Regulating Cardiac Fibrosis: Erratum.

Theranostics 2021 8;11(15):7618-7619. Epub 2021 Jun 8.

Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

[This corrects the article DOI: 10.7150/thno.15007.].
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http://dx.doi.org/10.7150/thno.63330DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8210619PMC
June 2021

Exercise attenuates angiotensinⅡ-induced muscle atrophy by targeting PPARγ/miR-29b.

J Sport Health Sci 2021 Jun 8. Epub 2021 Jun 8.

Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China; Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai 200444, China. Electronic address:

Background: Exercise is beneficial for muscle atrophy. Peroxisome proliferator-activated receptor gamma (PPARγ) and microRNA-29b (miR-29b) have been reported to be responsible for angiotensin Ⅱ (AngⅡ)-induced muscle atrophy. However, it is unclear whether exercise can protect AngⅡ-induced muscle atrophy by targeting PPARγ/miR-29b.

Methods: Skeletal muscle atrophy in both the control group and the run group was established by AngⅡ infusion; after 1 week of exercise training, the mice were sacrificed, and muscle weight was determined. Myofiber size was measured by hematoxylin-eosin and wheat-germ agglutinin staining. Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression level of muscle atrogenes, including F-box only protein 32 (FBXO32, also called Atrogin-1) and muscle-specific RING-finger 1 (MuRF-1), the phosphorylation level of protein kinase B (PKB, also called AKT)/forkhead box O3A (FOXO3A)/mammalian target of rapamycin (mTOR) pathway proteins, the expression level of PPARγ and apoptosis-related proteins, including B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X (Bax), cysteine-aspartic acid protease 3 (caspase-3), and cleaved-caspase-3, were determined by western blot. The expression level of miR-29b was checked by reverse-transcription quantitative polymerase chain reaction. A PPARγ inhibitor (T0070907) or adeno-associated virus serotype-8 (AAV8)-mediated miR-29b overexpression was used to demonstrate whether PPARγ activation or miR-29b inhibition mediates the beneficial effects of exercise in AngⅡ-induced muscle atrophy.

Results: Exercise can significantly attenuate AngⅡ-induced muscle atrophy, which is demonstrated by increased skeletal muscle weight, cross-sectional area of myofiber, and activation of AKT/mTOR signaling and by decreased atrogenes expressions and apoptosis. In AngⅡ-induced muscle atrophy mice models, PPARγ was elevated whereas miR-29b was decreased by exercise. The protective effects of exercise in AngⅡ-induced muscle atrophy were inhibited by a PPARγ inhibitor (T0070907) or adeno-associated virus serotype-8 (AAV8)-mediated miR-29b overexpression.

Conclusion: Exercise attenuates AngⅡ-induced muscle atrophy by activation of PPARγ and suppression of miR-29b.
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http://dx.doi.org/10.1016/j.jshs.2021.06.002DOI Listing
June 2021

Long Noncoding RNA Cardiac Physiological Hypertrophy-Associated Regulator Induces Cardiac Physiological Hypertrophy and Promotes Functional Recovery After Myocardial Ischemia-Reperfusion Injury.

Circulation 2021 07 21;144(4):303-317. Epub 2021 May 21.

Shanghai Engineering Research Center of Organ Repair, School of Medicine (L.W., Y.B., J.W., Q.Z., J.X.), Shanghai University, China.

Background: The benefits of exercise training in the cardiovascular system have been well accepted; however, the underlying mechanism remains to be explored. Here, we report the initial functional characterization of an exercise-induced cardiac physiological hypertrophy-associated novel long noncoding RNA (lncRNA).

Methods: Using lncRNA microarray profiling, we identified lncRNAs in contributing the modulation of exercise-induced cardiac growth that we termed cardiac physiological hypertrophy-associated regulator (CPhar). Mice with adeno-associated virus serotype 9 driving CPhar overexpression and knockdown were used in in vivo experiments. Swim training was used to induce physiological cardiac hypertrophy in mice, and ischemia reperfusion injury surgery was conducted to investigate the protective effects of CPhar in mice. To investigate the mechanisms of CPhar's function, we performed various analyses including quantitative reverse transcription polymerase chain reaction, Western blot, histology, cardiac function (by echocardiography), functional rescue experiments, mass spectrometry, in vitro RNA transcription, RNA pulldown, RNA immunoprecipitation, chromatin immunoprecipitation assay, luciferase reporter assay, and coimmunoprecipitation assays.

Results: We screened the lncRNAs in contributing the modulation of exercise-induced cardiac growth through lncRNA microarray profiling and found that CPhar was increased with exercise and was necessary for exercise-induced physiological cardiac growth. The gain and loss of function of CPhar regulated the expression of proliferation markers, hypertrophy, and apoptosis in cultured neonatal mouse cardiomyocytes. Overexpression of CPhar prevented myocardial ischemia reperfusion injury and cardiac dysfunction in vivo. We identified DDX17 (DEAD-Box Helicase 17) as a binding partner of CPhar in regulating CPhar downstream factor ATF7 (activating transcription factor 7) by sequestering C/EBPβ (CCAAT/enhancer binding protein beta).

Conclusions: Our study of this lncRNA CPhar provides new insights into the regulation of exercise-induced cardiac physiological growth, demonstrating the cardioprotective role of CPhar in the heart, and expanding our mechanistic understanding of lncRNA function, as well.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.120.050446DOI Listing
July 2021

A Call to Action for New Global Approaches to Cardiovascular Disease Drug Solutions.

Circulation 2021 07 20;144(2):159-169. Epub 2021 Apr 20.

Universite´ de Lorraine, INSERM CIC 1493, INI CRCT, CHRU, Nancy, France (F.Z.).

While we continue to wrestle with the immense challenge of implementing equitable access to established evidence-based treatments, substantial gaps remain in our pharmacotherapy armament for common forms of cardiovascular disease including coronary and peripheral arterial disease, heart failure, hypertension, and arrhythmia. We need to continue to invest in the development of new approaches for the discovery, rigorous assessment, and implementation of new therapies. Currently, the time and cost to progress from lead compound/product identification to the clinic, and the success rate in getting there reduces the incentive for industry to invest, despite the enormous burden of disease and potential size of market. There are tremendous opportunities with improved phenotyping of patients currently batched together in syndromic "buckets." Use of advanced imaging and molecular markers may allow stratification of patients in a manner more aligned to biological mechanisms that can, in turn, be targeted by specific approaches developed using high-throughput molecular technologies. Unbiased "omic" approaches enhance the possibility of discovering completely new mechanisms in such groups. Furthermore, advances in drug discovery platforms, and models to study efficacy and toxicity more relevant to the human disease, are valuable. Re-imagining the relationships among discovery, translation, evaluation, and implementation will help reverse the trend away from investment in the cardiovascular space, establishing innovative platforms and approaches across the full spectrum of therapeutic development.
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http://dx.doi.org/10.1161/CIR.0000000000000981DOI Listing
July 2021

A call to action for new global approaches to cardiovascular disease drug solutions.

Eur Heart J 2021 04;42(15):1464-1475

Université de Lorraine, INSERM CIC 1493, INI CRCT, CHRU Nancy, France.

Whilst we continue to wrestle with the immense challenge of implementing equitable access to established evidence-based treatments, substantial gaps remain in our pharmacotherapy armament for common forms of cardiovascular disease including coronary and peripheral arterial disease, heart failure, hypertension, and arrhythmia. We need to continue to invest in the development of new approaches for the discovery, rigorous assessment, and implementation of new therapies. Currently, the time and cost to progress from lead compound/product identification to the clinic, and the success rate in getting there reduces the incentive for industry to invest, despite the enormous burden of disease and potential size of market. There are tremendous opportunities with improved phenotyping of patients currently batched together in syndromic 'buckets'. Use of advanced imaging and molecular markers may allow stratification of patients in a manner more aligned to biological mechanisms that can, in turn, be targeted by specific approaches developed using high-throughput molecular technologies. Unbiased 'omic' approaches enhance the possibility of discovering completely new mechanisms in such groups. Furthermore, advances in drug discovery platforms, and models to study efficacy and toxicity more relevant to the human disease, are valuable. Re-imagining the relationships among discovery, translation, evaluation, and implementation will help reverse the trend away from investment in the cardiovascular space, establishing innovative platforms and approaches across the full spectrum of therapeutic development.
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http://dx.doi.org/10.1093/eurheartj/ehab068DOI Listing
April 2021

Targets identified from exercised heart: killing multiple birds with one stone.

NPJ Regen Med 2021 Apr 9;6(1):23. Epub 2021 Apr 9.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong, China.

Cardiovascular diseases (CVDs) are a major cause of mortality worldwide, which are mainly driven by factors such as aging, sedentary lifestyle, and excess alcohol use. Exercise targets several molecules and protects hearts against many of these physiological and pathological stimuli. Accordingly, it is widely recognized as an effective therapeutic strategy for CVD. To investigate the molecular mechanism of exercise in cardiac protection, we identify and describe several crucial targets identified from exercised hearts. These targets include insulin-like growth factor 1 (IGF1)-phosphatidylinositol 3 phosphate kinase (PI3K)/protein kinase B (AKT), transcription factor CCAAT/enhancer-binding protein β (C/EBPβ), cardiac microRNAs (miRNAs, miR-222 and miR-17-3p etc.), exosomal-miRNAs (miR-342, miR-29, etc.), Sirtuin 1 (SIRT1), and nuclear factor erythroid 2‑related factor/metallothioneins (Nrf2/Mts). Targets identified from exercised hearts can alleviate injury via multiple avenues, including: (1) promoting cardiomyocyte proliferation; (2) facilitating cardiomyocyte growth and physiologic hypertrophy; (3) elevating the anti-apoptotic capacity of cardiomyocytes; (4) improving vascular endothelial function; (5) inhibiting pathological remodeling and fibrosis; (6) promoting extracellular vesicles (EVs) production and exosomal-molecules transfer. Exercise is one treatment ('stone'), which is cardioprotective via multiple avenues ('birds'), and is considered 'killing multiple birds with one stone' in this review. Further, we discuss the potential application of EV cargos in CVD treatment. We provide an outline of targets identified from the exercised heart and their mechanisms, as well as novel ideas for CVD treatment, which may provide novel direction for preclinical trials in cardiac rehabilitation.
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http://dx.doi.org/10.1038/s41536-021-00128-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8035363PMC
April 2021

miR-132/212 Impairs Cardiomyocytes Contractility in the Failing Heart by Suppressing SERCA2a.

Front Cardiovasc Med 2021 19;8:592362. Epub 2021 Mar 19.

Experimental Cardiology Laboratory, Division Heart and Lungs, Department of Cardiology, University Medical Center Utrecht, Utrecht, Netherlands.

Compromised cardiac function is a hallmark for heart failure, mostly appearing as decreased contractile capacity due to dysregulated calcium handling. Unfortunately, the underlying mechanism causing impaired calcium handling is still not fully understood. Previously the miR-132/212 family was identified as a regulator of cardiac function in the failing mouse heart, and pharmaceutically inhibition of miR-132 is beneficial for heart failure. In this study, we further investigated the molecular mechanisms of miR-132/212 in modulating cardiomyocyte contractility in the context of the pathological progression of heart failure. We found that upregulated miR-132/212 expressions in all examined hypertrophic heart failure mice models. The overexpression of miR-132/212 prolongs calcium decay in isolated neonatal rat cardiomyocytes, whereas cardiomyocytes isolated from miR-132/212 KO mice display enhanced contractility in comparison to wild type controls. In response to chronic pressure-overload, miR-132/212 KO mice exhibited a blunted deterioration of cardiac function. Using a combination of biochemical approaches and assays, we confirmed that miR-132/212 regulates SERCA2a by targeting the 3'-end untranslated region of SERCA2a. Additionally, we also confirmed PTEN as a direct target of miR-132/212 and potentially participates in the cardiac response to miR132/212. In end-stage heart failure patients, miR-132/212 is upregulated and correlates with reduced SERCA2a expression. The up-regulation of miR-132/212 in heart failure impairs cardiac contractile function by targeting SERCA2a, suggesting that pharmaceutical inhibition of miR-132/212 might be a promising therapeutic approach to promote cardiac function in heart failure patients.
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http://dx.doi.org/10.3389/fcvm.2021.592362DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8017124PMC
March 2021

High-Fat/High-Sugar Diet Causes Metabolic Disorders and Cardiac Dysfunction: a New Model in Primates.

J Cardiovasc Transl Res 2021 12 15;14(6):1019-1020. Epub 2021 Mar 15.

Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong, 226011, China.

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http://dx.doi.org/10.1007/s12265-021-10119-7DOI Listing
December 2021

Angiotensin II-induced muscle atrophy via PPARγ suppression is mediated by miR-29b.

Mol Ther Nucleic Acids 2021 Mar 25;23:743-756. Epub 2020 Dec 25.

Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.

The activation of the renin-angiotensin system (RAS) induced by increased angiotensin II (AngII) levels has been implicated in muscle atrophy, which is involved in the pathogenesis of congestive heart failure. Although peroxisome proliferator-activated receptor gamma (PPARγ) activation can suppress RAS, the exact role of PPARγ in AngII-induced muscle atrophy is unclear. Here we identified PPARγ as a negative regulator of miR-29b, a microRNA that is able to promote multiple types of muscle atrophy. Suppression of miR-29b could prevent AngII-induced muscle atrophy both and . IGF1, PI3K(p85α), and Yin Yang 1 (YY1) were identified as target genes of miR-29b, and overexpression of these targets could rescue AngII-induced muscle atrophy. Importantly, inhibition of PPARγ was sufficient to induce muscle atrophy, while PPARγ overexpression could attenuate that. These data indicate that the PPARγ/miR-29b axis mediates AngII-induced muscle atrophy, and increasing PPARγ or inhibiting miR-29b represents a promising approach to counteract AngII-induced muscle atrophy.
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http://dx.doi.org/10.1016/j.omtn.2020.12.015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868689PMC
March 2021

Inhibition of lncRNA MAAT Controls Multiple Types of Muscle Atrophy by cis- and trans-Regulatory Actions.

Mol Ther 2021 03 3;29(3):1102-1119. Epub 2020 Dec 3.

Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Sciences, Shanghai University, Shanghai 200444, China; School of Medicine, Shanghai University, Shanghai 200444, China. Electronic address:

Muscle atrophy is associated with negative outcomes in a variety of diseases. Identification of a common therapeutic target would address a significant unmet clinical need. Here, we identify a long non-coding RNA (lncRNA) (muscle-atrophy-associated transcript, lncMAAT) as a common regulator of skeletal muscle atrophy. lncMAAT is downregulated in multiple types of muscle-atrophy models both in vivo (denervation, Angiotensin II [AngII], fasting, immobilization, and aging-induced muscle atrophy) and in vitro (AngII, HO, and tumor necrosis factor alpha [TNF-α]-induced muscle atrophy). Gain- and loss-of-function analysis both in vitro and in vivo reveals that downregulation of lncMAAT is sufficient to induce muscle atrophy, while overexpression of lncMAAT can ameliorate multiple types of muscle atrophy. Mechanistically, lncMAAT negatively regulates the transcription of miR-29b through SOX6 by a trans-regulatory module and increases the expression of the neighboring gene Mbnl1 by a cis-regulatory module. Therefore, overexpression of lncMAAT may represent a promising therapy for muscle atrophy induced by different stimuli.
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http://dx.doi.org/10.1016/j.ymthe.2020.12.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7934634PMC
March 2021

PPARγ agonists delay age-associated metabolic disease and extend longevity.

Aging Cell 2020 11 21;19(11):e13267. Epub 2020 Nov 21.

Division of Endocrinology, Diabetes and Metabolism, NYU Grossman School of Medicine, New York, NY, USA.

Aging leads to a number of disorders caused by cellular senescence, tissue damage, and organ dysfunction. It has been reported that anti-inflammatory and insulin-sensitizing compounds delay, or reverse, the aging process and prevent metabolic disorders, neurodegenerative disease, and muscle atrophy, improving healthspan and extending lifespan. Here we investigated the effects of PPARγ agonists in preventing aging and increasing longevity, given their known properties in lowering inflammation and decreasing glycemia. Our molecular and physiological studies show that long-term treatment of mice at 14 months of age with low doses of the PPARγ ligand rosiglitazone (Rosi) improved glucose metabolism and mitochondrial functionality. These effects were associated with decreased inflammation and reduced tissue atrophy, improved cognitive function, and diminished anxiety- and depression-like conditions, without any adverse effects on cardiac and skeletal functionality. Furthermore, Rosi treatment of mice started when they were 14 months old was associated with lifespan extension. A retrospective analysis of the effects of the PPARγ agonist pioglitazone (Pio) on longevity showed decreased mortality in patients receiving Pio compared to those receiving a PPARγ-independent insulin secretagogue glimepiride. Taken together, these data suggest the possibility of using PPARγ agonists to promote healthy aging and extend lifespan.
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http://dx.doi.org/10.1111/acel.13267DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7681041PMC
November 2020

Current Studies and Future Directions of Exercise Therapy for Muscle Atrophy Induced by Heart Failure.

Front Cardiovasc Med 2020 23;7:593429. Epub 2020 Oct 23.

Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai, China.

Muscle atrophy is a common complication of heart failure. At present, there is no specific treatment to reverse the course of muscle atrophy. Exercise training, due to the safety and easy operation, is a recommended therapy for muscle atrophy induced by heart failure. However, the patients with muscle atrophy are weak in mobility and may not be able to train for a long time. Therefore, it is necessary to explore novel targets of exercise protection for muscle atrophy, so as to improve the quality of life and survival rate of patients with muscular atrophy induced by heart failure. This article aims to review latest studies, summarize the evidence and limitations, and provide a glimpse into the future of exercise for the treatment of muscle atrophy induced by heart failure. We wish to highlight some important findings about the essential roles of exercise sensors in muscle atrophy induced by heart failure, which might be helpful for searching potential therapeutic targets for muscle wasting induced by heart failure.
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http://dx.doi.org/10.3389/fcvm.2020.593429DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7644508PMC
October 2020

Editorial: MicroRNA Signaling.

Front Cell Dev Biol 2020 30;8:612425. Epub 2020 Oct 30.

Alessandrescu-Rusescu National Institute of Mother and Child Health, Fetal Medicine Excellence Research Center, Bucharest, Romania.

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http://dx.doi.org/10.3389/fcell.2020.612425DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7661383PMC
October 2020

MiRNAs: A Powerful Tool in Deciphering Gynecological Malignancies.

Front Oncol 2020 23;10:591181. Epub 2020 Oct 23.

Department of General Surgery, Sf. Maria Clinical Hospital, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.

Accumulated evidence on the clinical roles of microRNAs (miRNAs) in cancer prevention and control has revealed the emergence of new genetic techniques that have improved the understanding of the mechanisms essential for pathology induction and progression. Comprehension of the modifications and individual differences of miRNAs and their interactions in the pathogenesis of gynecological malignancies, together with an understanding of the phenotypic variations have considerably improved the management of the diagnosis and personalized treatment for different forms of cancer. In recent years, miRNAs have emerged as signaling molecules in biological pathways involved in different categories of cancer and it has been demonstrated that these molecules could regulate cancer-relevant processes, our focus being on malignancies of the gynecologic tract. The aim of this paper is to summarize novel research findings in the literature regarding the parts that miRNAs play in cancer-relevant processes, specifically regarding gynecological malignancy, while emphasizing their pivotal role in the disruption of cancer-related signaling pathways.
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http://dx.doi.org/10.3389/fonc.2020.591181DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646292PMC
October 2020

Mir-30d Regulates Cardiac Remodeling by Intracellular and Paracrine Signaling.

Circ Res 2021 01 22;128(1):e1-e23. Epub 2020 Oct 22.

Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School, Boston (A.M.S., G.L., N.V., O.Z., A.Y., C.Y.X., R.S.R., PK., M.G.S., R.K., R.S., S.D.).

Rationale: Previous translational studies implicate plasma extracellular microRNA-30d (miR-30d) as a biomarker in left ventricular remodeling and clinical outcome in heart failure (HF) patients, although precise mechanisms remain obscure.

Objective: To investigate the mechanism of miR-30d-mediated cardioprotection in HF.

Methods And Results: In rat and mouse models of ischemic HF, we show that miR-30d gain of function (genetic, lentivirus, or agomiR-mediated) improves cardiac function, decreases myocardial fibrosis, and attenuates cardiomyocyte (CM) apoptosis. Genetic or locked nucleic acid-based knock-down of miR-30d expression potentiates pathological left ventricular remodeling, with increased dysfunction, fibrosis, and cardiomyocyte death. RNA sequencing of in vitro miR-30d gain and loss of function, together with bioinformatic prediction and experimental validation in cardiac myocytes and fibroblasts, were used to identify and validate direct targets of miR-30d. miR-30d expression is selectively enriched in cardiomyocytes, induced by hypoxic stress and is acutely protective, targeting MAP4K4 (mitogen-associate protein kinase 4) to ameliorate apoptosis. Moreover, miR-30d is secreted primarily in extracellular vesicles by cardiomyocytes and inhibits fibroblast proliferation and activation by directly targeting integrin α5 in the acute phase via paracrine signaling to cardiac fibroblasts. In the chronic phase of ischemic remodeling, lower expression of miR-30d in the heart and plasma extracellular vesicles is associated with adverse remodeling in rodent models and human subjects and is linked to whole-blood expression of genes implicated in fibrosis and inflammation, consistent with observations in model systems.

Conclusions: These findings provide the mechanistic underpinning for the cardioprotective association of miR-30d in human HF. More broadly, our findings support an emerging paradigm involving intercellular communication of extracellular vesicle-contained miRNAs (microRNAs) to transregulate distinct signaling pathways across cell types. Functionally validated RNA biomarkers and their signaling networks may warrant further investigation as novel therapeutic targets in HF.
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http://dx.doi.org/10.1161/CIRCRESAHA.120.317244DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7790887PMC
January 2021

Sheng-Mai Yin exerts anti-inflammatory effects on RAW 264.7 cells and zebrafish.

J Ethnopharmacol 2021 Mar 19;267:113497. Epub 2020 Oct 19.

Traditional Chinese Pharmacological Laboratory, Third Level Research Laboratory of State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, PR China; Guangdong Provincial Key Laboratory of Chinese Medicine Pharmaceutics, Guangzhou, 510515, PR China. Electronic address:

Ethnopharmacological Relevance: Sheng-Mai Yin (SMY), a famous traditional Chinese medicine formula, has been commonly used in China for centuries to treat various diseases, such as inflammation-related diseases. However, the anti-inflammatory activity of SMY and its potential mechanisms still have not yet been clearly understood.

Aim Of The Study: In this study, we aimed to determine the anti-inflammatory effect of SMY and explore its underlying mechanisms both on RAW 264.7 cells and zebrafish.

Materials And Methods: The levels of pro-inflammatory cytokines IL-6 and TNF-α secreted by RAW 264.7 cells were measured by ELISA. The protein expressions of IκBα, p-IκBα (Ser32), STAT3 and p-STAT3 (Tyr705) were determined by Western blotting. And the nuclear translocation of NF-κB p65 in LPS-induced RAW 264.7 macrophage cells was detected by confocal microscopy. Moreover, the in vivo anti-inflammatory effect of SMY and its potential mechanisms were further investigated by survival analysis, hematoxylin-eosin staining (H&E), observation of neutrophil migration and quantitative real-time PCR (qRT-PCR) analysis in zebrafish inflammatory models.

Results: SMY reduced the release of IL-6 and TNF-α, inhibited the phosphorylation of IκBα and STAT3 as well as the nuclear translocation of NF-κB p65 in LPS-induced RAW 264.7 cells. Furthermore, the increased survival, decreased infiltration of inflammatory cells and the attenuated migration of neutrophils together suggested the in vivo anti-inflammatory effects of SMY. More importantly, SMY reduced the gene expressions of pro-inflammatory cytokines and suppressed LPS-induced up-regulation of NF-κB, IκBα and STAT3 in zebrafish inflammatory models.

Conclusion: SMY exerts significant anti-inflammatory effects with a potential mechanism of inhibiting the NF-κB and STAT3 signal pathways. Our findings suggest a scientific rationale of SMY to treat inflammatory diseases in clinic.
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http://dx.doi.org/10.1016/j.jep.2020.113497DOI Listing
March 2021

Cellular and Molecular Mechanism of Cardiac Regeneration: A Comparison of Newts, Zebrafish, and Mammals.

Biomolecules 2020 08 19;10(9). Epub 2020 Aug 19.

Department of Cardiology, Experimental Cardiology Laboratory, UMC Utrecht, 3584CX Utrecht, The Netherlands.

Cardiovascular disease is the leading cause of death worldwide. Current palliative treatments can slow the progression of heart failure, but ultimately, the only curative treatment for end-stage heart failure is heart transplantation, which is only available for a minority of patients due to lack of donors' hearts. Explorative research has shown the replacement of the damaged and lost myocardium by inducing cardiac regeneration from preexisting myocardial cells. Lower vertebrates, such as the newt and zebrafish, can regenerate lost myocardium through cardiomyocyte proliferation. The preexisting adult cardiomyocytes replace the lost cells through subsequent dedifferentiation, proliferation, migration, and re-differentiation. Similarly, neonatal mice show complete cardiac regeneration post-injury; however, this regenerative capacity is remarkably diminished one week after birth. In contrast, the adult mammalian heart presents a fibrotic rather than a regenerative response and only shows signs of partial pathological cardiomyocyte dedifferentiation after injury. In this review, we explore the cellular and molecular responses to myocardial insults in different adult species to give insights for future interventional directions by which one can promote or activate cardiac regeneration in mammals.
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http://dx.doi.org/10.3390/biom10091204DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564143PMC
August 2020

Noncoding RNAs in Cardiovascular Disease: Current Knowledge, Tools and Technologies for Investigation, and Future Directions: A Scientific Statement From the American Heart Association.

Circ Genom Precis Med 2020 08 29;13(4):e000062. Epub 2020 Jun 29.

Background: The discovery that much of the non-protein-coding genome is transcribed and plays a diverse functional role in fundamental cellular processes has led to an explosion in the development of tools and technologies to investigate the role of these noncoding RNAs in cardiovascular health. Furthermore, identifying noncoding RNAs for targeted therapeutics to treat cardiovascular disease is an emerging area of research. The purpose of this statement is to review existing literature, offer guidance on tools and technologies currently available to study noncoding RNAs, and identify areas of unmet need.

Methods: The writing group used systematic literature reviews (including MEDLINE, Web of Science through 2018), expert opinion/statements, analyses of databases and computational tools/algorithms, and review of current clinical trials to provide a broad consensus on the current state of the art in noncoding RNA in cardiovascular disease.

Results: Significant progress has been made since the initial studies focusing on the role of miRNAs (microRNAs) in cardiovascular development and disease. Notably, recent progress on understanding the role of novel types of noncoding small RNAs such as snoRNAs (small nucleolar RNAs), tRNA (transfer RNA) fragments, and Y-RNAs in cellular processes has revealed a noncanonical function for many of these molecules. Similarly, the identification of long noncoding RNAs that appear to play an important role in cardiovascular disease processes, coupled with the development of tools to characterize their interacting partners, has led to significant mechanistic insight. Finally, recent work has characterized the unique role of extracellular RNAs in mediating intercellular communication and their potential role as biomarkers.

Conclusions: The rapid expansion of tools and pipelines for isolating, measuring, and annotating these entities suggests that caution in interpreting results is warranted until these methodologies are rigorously validated. Most investigators have focused on investigating the functional role of single RNA entities, but studies suggest complex interaction between different RNA molecules. The use of network approaches and advanced computational tools to understand the interaction of different noncoding RNA species to mediate a particular phenotype may be required to fully comprehend the function of noncoding RNAs in mediating disease phenotypes.
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http://dx.doi.org/10.1161/HCG.0000000000000062DOI Listing
August 2020

Exosomes: Multifaceted Messengers in Atherosclerosis.

Curr Atheroscler Rep 2020 08 9;22(10):57. Epub 2020 Aug 9.

Cardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, 333 Nan Chen Road, Shanghai, 200444, China.

Purpose Of Review: Atherosclerosis (AS) is a chronic inflammatory disease that contributes to the development of coronary artery disease, which has become a leading health burden worldwide. Though several strategies such as pharmacological treatment, exercise intervention, and surgery have been used in clinical practice, there is still no effective strategy to cure AS. Exosomes are extensively studied both as diagnostic markers as well as for therapeutic purposes due to their role in pathological processes related to AS. To elucidate the role of exosomes in AS and thus provide a new insight into AS therapy, we review recent advances concerning exosome targets and their function in mediating intercellular communication in AS, and expect to provide a reference for novel effective strategies to cure AS.

Recent Findings: Exosomes exert important roles in the diagnosis, development, and potential therapy of AS. For AS development, (1) activation of CD-137 in endothelial cells represses exosomal-TET2 production, causing a phenotypic switch of vascular smooth muscle cells (VSMC) and promoting plaque formation; (2) exosomal-MALTA1 derived from endothelial cells causes neutrophil extracellular traps (NETs) and M2 macrophage polarization, which aggravates AS; and (3) exosomal-miR-21-3p derived from macrophages inhibits PTEN expression and further promotes VSMC migration/proliferation, leading to AS development. For AS diagnosis, plasma exosomal-miR30e and miR-92a are considered to be potential diagnostic markers. For AS therapy, adipose mesenchymal stem cell-derived exosomes protect endothelial cells from AS aggravation, via inhibiting miR-342-5p. Exosome-mediated cross-talk between different cells within the vasculature exerts crucial roles in regulating endothelial function, proliferation and differentiation of vascular smooth muscle cells, and platelet activation as well as macrophage activation, collectively leading to the development and progression of AS. Exosomes can potentially be used as diagnostic biomarkers and constitute as a new therapeutic strategy for AS.
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http://dx.doi.org/10.1007/s11883-020-00871-7DOI Listing
August 2020

FEM simulation and comparison of PMN-PT single crystals based phased array ultrasonic transducer by alternating current poling and direct current poling.

Ultrasonics 2020 Dec 24;108:106175. Epub 2020 May 24.

Artificial Crystal Research Center, Shanghai Institute of Ceramics, Chinese Academy of Sciences, 215 Chengbei Road, Jiading, Shanghai 201800, China; Center of Materials Science and Optoelectronics Engineering, University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:

The Finite element modeling (FEM) simulation and comparison of electroacoustic properties for alternating current poling (ACP) phased arrays and direct current poling (DCP) phased arrays were investigated. The simulated electrical impedance reveals that the effective working bandwidth of ACP phased arrays is wider than that of DCP phased arrays as a whole. Besides, the ACP phased arrays have a higher effective electromechanical coupling coefficient k compared to DCP arrays, which indicates that higher electromechanical conversion capacity is obtained. The average value of the ratio of longitudinal displacement R for ACP phased arrays is larger than that of DCP arrays, indicating that the longitudinal transmission efficiency of acoustic energy can be enhanced by using the ACP method. The simulation results of crosstalk are consistent with the results of vibration modal analysis. The coupling effect of transverse vibration for ACP phased arrays is weaker than that of DCP arrays, leading to reduce the interaction between the adjacent elements. The crosstalk of the ACP arrays is -11.87 dB, 0.91 dB lower than that of DCP arrays. The pulse-echo response of ACP phased arrays is 7.2% broader -6 dB bandwidth, 0.79 dB higher relative sensitivity compared to the DCP phased arrays, which prove that the longitudinal resolution and penetration depth of the ultrasonic imaging can be improved by using the ACP arrays. Besides, the consequences of the beam profile illustrate that the maximum acoustic pressure of ACP arrays is 13.8% higher than that of DCP arrays and the directivity of ACP array is slightly better than that of DCP arrays.
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http://dx.doi.org/10.1016/j.ultras.2020.106175DOI Listing
December 2020
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