8,226 results match your criteria Journal of molecular and cellular cardiology[Journal]


Matrix metalloproteinase-12 produced by Ly6C macrophages prolongs the survival after myocardial infarction by preventing neutrophil influx.

J Mol Cell Cardiol 2019 Apr 19. Epub 2019 Apr 19.

Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan. Electronic address:

Background: Various immune cells are involved in different phases of cardiac repair after myocardial infarction (MI). Especially, Ly6C M2-like macrophages (Ly6C macrophages) are vital for cardiac repair after MI. However, the molecular mechanisms how Ly6C macrophages promote wound healing after MI are still largely unknown. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.007DOI Listing

Knockout of adenylyl cyclase isoform 5 or 6 differentially modifies the β-adrenoceptor-mediated inotropic response.

J Mol Cell Cardiol 2019 Apr 19. Epub 2019 Apr 19.

Faculty of Medicine, Department of Pharmacology, Center for Heart Failure Research, Oslo University Hospital, University of Oslo, Oslo, Norway.

Although only β-adrenergic receptors (βAR) dually couple with stimulatory G protein (G) and inhibitory G protein (G), inactivation of G enhances both βAR and βAR responsiveness. We hypothesize that G restrains spontaneous adenylyl cyclase (AC) activity independent of receptor activation. Subcellular localization of the AC5/6 subtypes varies contributing to the compartmentation of βAR signaling. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.017DOI Listing

The role of fibroblast - Cardiomyocyte interaction for atrial dysfunction in HFpEF and hypertensive heart disease.

J Mol Cell Cardiol 2019 Apr 18. Epub 2019 Apr 18.

Department of Internal Medicine and Cardiology, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburgerplatz 1, 13353 Berlin, Germany; DZHK (German Centre for Cardiovascular Research), partner site Berlin, Germany; Berlin Institute of Health (BIH), Berlin, Germany. Electronic address:

Aims: Atrial contractile dysfunction is associated with increased mortality in heart failure (HF). We have shown previously that a metabolic syndrome-based model of HFpEF and a model of hypertensive heart disease (HHD) have impaired left atrial (LA) function in vivo (rat). In this study we postulate, that left atrial cardiomyocyte (CM) and cardiac fibroblast (CF) paracrine interaction related to the inositol 1,4,5-trisphosphate signalling cascade is pivotal for the manifestation of atrial mechanical dysfunction in HF and that quantitative atrial remodeling is highly disease-dependent. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.016DOI Listing

Heparanase protects the heart against chemical or ischemia/reperfusion injury.

J Mol Cell Cardiol 2019 Apr 17. Epub 2019 Apr 17.

Faculty of Pharmaceutical Sciences, University of British Columbia, 2405 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada. Electronic address:

Although cancer cells use heparanase for tumor metastasis, favourable effects of heparanase have been reported in the management of Alzheimer's disease and diabetes. Indeed, we previously established a protective function for heparanase in the acutely diabetic heart, where it conferred cardiomyocyte resistance to oxidative stress and apoptosis by provoking changes in gene expression. In this study, we tested if overexpression of heparanase can protect the heart against chemically induced or ischemia/reperfusion (I/R) injury. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.008DOI Listing

Downregulation of ATR decreases the responsiveness of BK channels to angiotensin II in patients with hypertension.

J Mol Cell Cardiol 2019 Apr 15. Epub 2019 Apr 15.

Key Lab of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Lab of Sichuan Province, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, Luzhou, Sichuan 646000, China. Electronic address:

Angiotensin II (Ang II) modulates blood pressure via Ang II type 1 receptor (ATR) and type 2 receptor (ATR). The activation of ATR relaxes vascular tone through opening large-conductance Ca-activated potassium (BK) channels in vascular smooth muscle cells (SMCs). In the present study, we studied the role of the ATR-BK pathway in patients with hypertension. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.013DOI Listing

The assembly and evaluation of antisense oligonucleotides applied in exon skipping for titin-based mutations in dilated cardiomyopathy.

J Mol Cell Cardiol 2019 Apr 15. Epub 2019 Apr 15.

Department of Cardiology and Cardiovascular Diseases, Eberhard Karls University, Tübingen, Germany; Department of Cardiology, RWTH Aachen, Pauwelsstr. 30, Aachen, Germany. Electronic address:

The leading cause of genetic dilated cardiomyopathy (DCM) is due to mutations in the TTN gene, impacting approximately 15-20% of familial and 18% of sporadic DCM cases. Currently, there is potential for a personalized RNA-based therapeutic approach in titin-based DCM, utilizing antisense oligonucleotide (AON) mediated exon-skipping, which attempts to reframe mutated titin transcripts, resulting in shortened, functional protein. However, the TTN gene is massive with 363 exons; each newly identified TTN exon mutation provides a challenge to address when considering the potential application of AON mediated exon skipping. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828193003
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http://dx.doi.org/10.1016/j.yjmcc.2019.04.014DOI Listing
April 2019
2 Reads

Yin-Yang 1 transcription factor modulates ST2 expression during adverse cardiac remodeling post-myocardial infarction.

J Mol Cell Cardiol 2019 Apr 15;130:216-233. Epub 2019 Apr 15.

Cardiology Department, Clinic and Universitary Hospital Virgen de la Arrixaca, Murcia, Spain; CIBER in Cardiovascular Diseases (CIBERCV), Madrid, Spain.

Background: The cardioprotective effects of metformin remain poorly defined. Interleukin (IL)-33/ST2L signaling is a novel cardioprotective pathway, which is antagonized by the soluble isoform sST2. No data exist about the regulation of ST2 expression. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.009DOI Listing

Identification of circumferential regional heterogeneity of ascending thoracic aneurysmal aorta by biaxial mechanical testing.

J Mol Cell Cardiol 2019 Apr 15;130:205-215. Epub 2019 Apr 15.

Department for the Treatment and Study of Cardiothoracic Diseases and Cardiothoracic Transplantation, IRCCS-ISMETT, Via Tricomi n.5, 90127 Palermo, Italy.

Ascending thoracic aortic aneurysm (ATAA) in patients with bicuspid aortic valve (BAV) can present an asymmetrical aortic dilatation compared with patients with tricuspid aortic valve (TAV). This pattern of aneurysm dilatation led us to hypothesize that biomechanical differences likely induced by regional heterogeneity of material properties can underlie the observed asymmetric enlargement discrepancies between BAV ATAA and TAV ATAA. This study aimed to characterize the mechanical properties and associated aortic tissue stiffness changes along the circumferential direction of aortic rings collected from surgically-repaired patients with ATAA. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.010DOI Listing
April 2019
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Activation of the PP2A catalytic subunit by ivabradine attenuates the development of diabetic cardiomyopathy.

J Mol Cell Cardiol 2019 Apr 15;130:170-183. Epub 2019 Apr 15.

Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China. Electronic address:

Hyperglycemia-induced apoptosis plays a critical role in the pathogenesis of diabetic cardiomyopathy (DCM). Our previous study demonstrated that ivabradine, a selective I current antagonist, significantly attenuated myocardial apoptosis in diabetic mice, but the underlying mechanisms remained unknown. This study investigated the underlying mechanisms by which ivabradine exerts anti-apoptotic effects in experimental DCM. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.011DOI Listing

LncRNA H19 promotes vascular inflammation and abdominal aortic aneurysm formation by functioning as a competing endogenous RNA.

J Mol Cell Cardiol 2019 Apr 13. Epub 2019 Apr 13.

State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address:

Abdominal aortic aneurysm (AAA) is accepted as a chronic vascular inflammatory disease. However, how the inflammatory response is regulated during AAA formation is not fully understood. This study was undertaken to determine whether the long noncoding RNA (lncRNA) H19 (H19) promotes AAA formation by enhancing aortic inflammation. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.004DOI Listing
April 2019
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Epigenetic therapies in heart failure.

J Mol Cell Cardiol 2019 Apr 13;130:197-204. Epub 2019 Apr 13.

Gladstone Institutes, San Francisco, CA, United States of America; Division of Cardiology, Department of Medicine, University of California San Francisco School of Medicine, San Francisco, CA, United States of America; Cardiometabolic Disorders, Amgen, South San Francisco, CA, United States of America. Electronic address:

Heart failure (HF) is a dominant cause of morbidity and mortality in the developed world, with available pharmacotherapies limited by high rates of residual mortality and a failure to directly target the changes in cell state that drive adverse cardiac remodeling. Pathologic cardiac remodeling is driven by stress-activated cardiac signaling cascades that converge on defined components of the chromatin regulatory apparatus in the nucleus, triggering broad shifts in transcription and cell state. Thus, studies focusing on how cytosolic signaling pathways couple to the nuclear gene control machinery has been an area of therapeutic interest in HF. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828193006
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http://dx.doi.org/10.1016/j.yjmcc.2019.04.012DOI Listing
April 2019
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A high-throughput ratiometric method for imaging hypertrophic growth in cultured primary cardiac myocytes.

J Mol Cell Cardiol 2019 Apr 13;130:184-196. Epub 2019 Apr 13.

University of Oxford, Department of Physiology, Anatomy & Genetics, Parks Road, Oxford OX1 3PT, United Kingdom. Electronic address:

Maladaptive hypertrophy of cardiac myocytes increases the risk of heart failure. The underlying signaling can be triggered and interrogated in cultured neonatal ventricular myocytes (NRVMs) using sophisticated pharmacological and genetic techniques. However, the methods for quantifying cell growth are, by comparison, inadequate. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.001DOI Listing

Biology, pathophysiology and current therapies that affect lipoprotein (a) levels.

J Mol Cell Cardiol 2019 Apr 12;131:1-11. Epub 2019 Apr 12.

School of Medical Sciences, Faculty of Medicine, UNSW Sydney, Sydney, NSW 2052, Australia. Electronic address:

Lipoprotein (a) [Lp(a)] has recently emerged as a causal, independent and genetic risk factor for cardiovascular disease and calcific aortic valve disease. Given the high incidence of elevated Lp(a) among the general population, significant gaps in the knowledge of Lp(a) biology, pathophysiology and current therapies affecting Lp(a) reduction exist. As plasma Lp(a) levels are genetically determined and insensible to diet, exercise and lifestyle changes, lipid-lowering therapies seem to be the solution to lower elevated Lp(a) levels. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183117
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http://dx.doi.org/10.1016/j.yjmcc.2019.04.005DOI Listing
April 2019
1 Read

Drp1/Fis1 interaction mediates mitochondrial dysfunction in septic cardiomyopathy.

J Mol Cell Cardiol 2019 Apr 11;130:160-169. Epub 2019 Apr 11.

Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA 94305, USA.

Mitochondrial dysfunction is a key contributor to septic cardiomyopathy. Although recent literature implicates dynamin related protein 1 (Drp1) and its mitochondrial adaptor fission 1 (Fis1) in the development of pathologic fission and mitochondrial failure in neurodegenerative disease, little is known about the role of Drp1/Fis1 interaction in the context of sepsis-induced cardiomyopathy. Our study tests the hypothesis that Drp1/Fis1 interaction is a major driver of sepsis-mediated pathologic fission, leading to mitochondrial dysfunction in the heart. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183119
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http://dx.doi.org/10.1016/j.yjmcc.2019.04.006DOI Listing
April 2019
3 Reads

Histone deacetylases in cardiovascular and metabolic diseases.

J Mol Cell Cardiol 2019 Apr 9;130:151-159. Epub 2019 Apr 9.

Baker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Diabetes, Central Clinical School, Monash University, Clayton, VIC 3800, Australia. Electronic address:

Histone deacetylases (HDACs) regulate gene transcription by catalyzing the removal of acetyl groups from key lysine residues in nucleosomal histones and via the recruitment of other epigenetic regulators to DNA promoter/enhancer regions. Over the past two decades, HDACs have been implicated in multiple processes pertinent to cardiovascular and metabolic diseases, including cardiac hypertrophy and remodeling, fibrosis, calcium handling, inflammation and energy metabolism. The development of small molecule HDAC inhibitors and genetically modified loss- and gain-of-function mouse models has allowed interrogation of the roles of specific HDAC isoforms in these processes. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183123
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http://dx.doi.org/10.1016/j.yjmcc.2019.04.003DOI Listing
April 2019
2 Reads

Supporting the heart: functions of the cardiomyocyte's non-sarcomeric cytoskeleton.

J Mol Cell Cardiol 2019 Apr 9. Epub 2019 Apr 9.

Heart, Lung and Vascular Institute, University of Cincinnati, Cincinnati, OH, USA.

The non-contractile cytoskeleton in cardiomyocytes is comprised of cytoplasmic actin, microtubules, and intermediate filaments. In addition to providing mechanical support to these cells, these structures are important effectors of tension-sensing and signal transduction and also provide networks for the transport of proteins and organelles. The majority of our knowledge on the function and structure of these cytoskeletal networks comes from research on proliferative cell types. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.04.002DOI Listing

C53: A novel particulate guanylyl cyclase B receptor activator that has sustained activity in vivo with anti-fibrotic actions in human cardiac and renal fibroblasts.

J Mol Cell Cardiol 2019 Apr 4;130:140-150. Epub 2019 Apr 4.

Cardiorenal Research Laboratory, Department of Cardiovascular Medicine, United States; Department of Physiology and Biomedical Engineering, United States. Electronic address:

The native particulate guanylyl cyclase B receptor (pGC-B) activator, C-type natriuretic peptide (CNP), induces anti-remodeling actions in the heart and kidney through the generation of the second messenger 3', 5' cyclic guanosine monophosphate (cGMP). Indeed fibrotic remodeling, particularly in cardiorenal disease states, contributes to disease progression and thus, has been a key target for drug discovery and development. Although the pGC-B/cGMP system has been perceived as a promising anti-fibrotic pathway, its therapeutic potential is limited due to the rapid degradation and catabolism of CNP by neprilysin (NEP) and natriuretic peptide clearance receptor (NPRC). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.024DOI Listing

Pressure overload inhibits glucocorticoid receptor transcriptional activity in cardiomyocytes and promotes pathological cardiac hypertrophy.

J Mol Cell Cardiol 2019 Apr 1;130:122-130. Epub 2019 Apr 1.

Department of Cardiology, Keio University School of Medicine, Tokyo, Japan. Electronic address:

Glucocorticoid receptor (GR) is abundantly expressed in cardiomyocytes. However, the role of GR in regulating cardiac hypertrophy and heart failure in response to pressure overload remains unclear. Cardiomyocyte-specific GR knockout (GRcKO) mice, mineralocorticoid receptor (MR) knockout (MRcKO), and GR and MR double KO (GRMRdcKO) mice were generated using the Cre-lox system. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.019DOI Listing
April 2019
2 Reads

Biased signaling of Ca-sensing receptors in cardiac myocytes regulates GIRK channel activity.

J Mol Cell Cardiol 2019 Mar 29;130:107-121. Epub 2019 Mar 29.

Department of Physiology, Ruhr University Bochum, Bochum, Germany.

Ca-sensing receptors (CaSRs) belong to the class C of G protein-coupled receptors and are activated by extracellular Ca. CaSRs display biased G protein signaling by coupling to different classes of heterotrimeric G proteins depending on agonist and cell type. In this study we used fluorescent biosensors to directly analyze G protein coupling to CaSRs and downstream signaling in living cells. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.022DOI Listing

Enhanced closed-state inactivation of mutant cardiac sodium channels (SCN5A N1541D and R1632C) through different mechanisms.

J Mol Cell Cardiol 2019 Mar 30;130:88-95. Epub 2019 Mar 30.

Department of Cardiovascular Medicine, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Background: SCN5A variants can be associated with overlapping phenotypes such as Brugada syndrome (BrS), sinus node dysfunction and supraventricular tachyarrhythmias. Our genetic screening of SCN5A in 65 consecutive BrS probands revealed two patients with overlapping phenotypes: one carried an SCN5A R1632C (in domain IV-segment 4), which we have previously reported, the other carried a novel SCN5A N1541D (in domain IV-segment 1).

Objective: We sought to reveal whether or not these variants are associated with the same biophysical defects. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.023DOI Listing

Smooth muscle-specific LKB1 deletion exaggerates angiotensin II-induced abdominal aortic aneurysm in mice.

J Mol Cell Cardiol 2019 Mar 30;130:131-139. Epub 2019 Mar 30.

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education,Chinese Ministry of Health and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, Shandong, China; School of Pharmacy, Hubei University of Science and Technology, Xianning, Hubei, China. Electronic address:

Abdominal aortic aneurysm (AAA) is a life-threatening vascular disease without an effective pharmaceutical treatment. Liver kinase B1 (LKB1), a tumor suppressor, is a central regulator of cell polarity and energy homeostasis. However, the role of LKB1 in the development of AAA has not been explored. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.021DOI Listing
March 2019
3 Reads

Calmodulin inhibition of human RyR2 channels requires phosphorylation of RyR2-S2808 or RyR2-S2814.

J Mol Cell Cardiol 2019 Mar 27;130:96-106. Epub 2019 Mar 27.

School of Biomedical Sciences and Pharmacy, University of Newcastle and Hunter Medical Research Institute, Callaghan, NSW 2308, Australia. Electronic address:

Calmodulin (CaM) is a Ca-binding protein that binds to, and can directly inhibit cardiac ryanodine receptor calcium release channels (RyR2). Animal studies have shown that RyR2 hyperphosphorylation reduces CaM binding to RyR2 in failing hearts, but data are lacking on how CaM regulates human RyR2 and how this regulation is affected by RyR2 phosphorylation. Physiological concentrations of CaM (100 nM) inhibited the diastolic activity of RyR2 isolated from failing human hearts by ~50% but had no effect on RyR2 from healthy human hearts. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.018DOI Listing
March 2019
2 Reads

CD146 deficiency promotes plaque formation in a mouse model of atherosclerosis by enhancing RANTES secretion and leukocyte recruitment.

J Mol Cell Cardiol 2019 Mar 27;130:76-87. Epub 2019 Mar 27.

Aix-Marseille Univ., INSERM 1263, INRA 1260, C2VN, Marseille, France. Electronic address:

Aims: The progression of atherosclerosis is based on the continued recruitment of leukocytes in the vessel wall. The previously described role of CD146 in leukocyte infiltration suggests an involvement for this adhesion molecule in the inflammatory response. In this study, we investigated the role of CD146 in leukocyte recruitment by using an experimental model of atherogenesis. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.017DOI Listing

Cardiomyocyte-GSK-3α promotes mPTP opening and heart failure in mice with chronic pressure overload.

J Mol Cell Cardiol 2019 Mar 27;130:65-75. Epub 2019 Mar 27.

Division of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

Chronic pressure-overload (PO)- induced cardiomyopathy is one of the leading causes of left ventricular (LV) remodeling and heart failure. The role of the α isoform of glycogen synthase kinase-3 (GSK-3α) in PO-induced cardiac remodeling is unclear and its downstream molecular targets are largely unknown. To investigate the potential roles of GSK-3α, cardiomyocyte-specific GSK-3α conditional knockout (cKO) and control mice underwent trans-aortic constriction (TAC) or sham surgeries. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.020DOI Listing

Adenosine kinase attenuates cardiomyocyte microtubule stabilization and protects against pressure overload-induced hypertrophy and LV dysfunction.

J Mol Cell Cardiol 2019 Mar 22;130:49-58. Epub 2019 Mar 22.

Department of Pharmacology and Toxicology, University of Graz, Graz 8010, Austria. Electronic address:

Adenosine exerts numerous protective actions in the heart, including attenuation of cardiac hypertrophy. Adenosine kinase (ADK) converts adenosine to adenosine monophosphate (AMP) and is the major route of myocardial adenosine metabolism, however, the impact of ADK activity on cardiac structure and function is unknown. To examine the role of ADK in cardiac homeostasis and adaptation to stress, conditional cardiomyocyte specific ADK knockout mice (cADK) were produced using the MerCreMer-lox-P system. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183112
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http://dx.doi.org/10.1016/j.yjmcc.2019.03.015DOI Listing
March 2019
13 Reads

Fluvastatin inhibits Rab5-mediated IKs internalization caused by chronic Ca-dependent PKC activation.

J Mol Cell Cardiol 2019 Mar 18;129:314-325. Epub 2019 Mar 18.

Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, United States of America. Electronic address:

Statins, in addition to their cholesterol lowering effects, can prevent isoprenylation of Rab GTPase proteins, a key protein family for the regulation of protein trafficking. Rab-GTPases have been shown to be involved in the control of membrane expression level of ion channels, including one of the major cardiac repolarizing channels, IKs. Decreased IKs function has been observed in a number of disease states and associated with increased propensity for arrhythmias, but the mechanism underlying IKs decrease remains elusive. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.016DOI Listing

Chronic inflammation: A key role in degeneration of bicuspid aortic valve.

J Mol Cell Cardiol 2019 Mar 15;130:59-64. Epub 2019 Mar 15.

Department of Excellence of Sciences for Health Promotion and Mothernal-Child Care, Internal Medicine and Specialities (PROMISE) "G. D'Alessandro", Italy; Cardiology Unit, University Hospital P. Giaccone, Palermo, Italy. Electronic address:

Introduction: Bicuspid aortic valve (BAV) is the most common congenital valvular heart defect resulting from abnormal aortic cusp formation during heart development, where two of the three normal and equal sized cusps fuse into a single large cusp resulting in a two cusps aortic valve. Over the past years, much interest has been given in understanding the pathogenesis of BAV and its complications. In this review, we focused on the role of inflammation, involved in the degeneration of BAV and the development of its complications. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.013DOI Listing
March 2019
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In vitro analysis of arrhythmogenic cardiomyopathy associated desmoglein-2 (DSG2) mutations reveals diverse glycosylation patterns.

J Mol Cell Cardiol 2019 Mar 15;129:303-313. Epub 2019 Mar 15.

Erich and Hanna Klessmann Institute for Cardiovascular Research and Development, Heart and Diabetes Center NRW, University Hospital of the Ruhr-University Bochum, Bad Oeynhausen, Germany.

Arrhythmogenic right ventricular cardiomyopathy is a heritable cardiac disease causing severe ventricular arrhythmias, heart failure and sudden cardiac death. It is mainly caused by mutations in genes encoding several structural proteins of the cardiac desmosomes including the DSG2 gene encoding the desmosomal cadherin desmoglein-2. Although the molecular structure of the extracellular domain of desmoglein-2 is known, it remains an open question, how mutations in DSG2 contribute to the pathogenesis of arrhythmogenic right ventricular cardiomyopathy. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.014DOI Listing
March 2019
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A dipeptidyl peptidase-IV inhibitor improves diastolic dysfunction in Dahl salt-sensitive rats.

J Mol Cell Cardiol 2019 Mar 14;129:257-265. Epub 2019 Mar 14.

Clinical Research and Development, National Cerebral and Cardiovascular Center, Osaka, Japan. Electronic address:

To date, there is no established treatment for heart failure with preserved ejection fraction (HFpEF). Dipeptidyl peptidase-IV (DPP-IV) inhibitors reportedly have improved not only diabetes mellitus but also heart failure with systolic dysfunction in experimental models. We investigated the effects of a DPP-IV inhibitor on HFpEF in rats. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.009DOI Listing

RNA epigenetics and cardiovascular diseases.

J Mol Cell Cardiol 2019 Mar 14;129:272-280. Epub 2019 Mar 14.

Department of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA. Electronic address:

Cardiovascular disease (CVD) remains the leading cause of death in the Western world. Despite advances in the prevention and in the management of CVD, the role of RNA epigenetics in the cardiovascular system has been until recently unexplored. The rapidly expanding research field of RNA modifications has introduced a novel layer of gene regulation in mammalian cells. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.010DOI Listing

Cardiovascular inflammation: RNA takes the lead.

J Mol Cell Cardiol 2019 Mar 14;129:247-256. Epub 2019 Mar 14.

Department of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, United States. Electronic address:

Inflammation has recently gained tremendous attention as a key contributor in several chronic diseases. While physiological inflammation is essential to counter a wide variety of damaging stimuli and to improve wound healing, dysregulated inflammation such as in the myocardium and vasculature can promote cardiovascular diseases. Given the high severity, prevalence, and economic burden of these diseases, understanding the factors involved in the regulation of physiological inflammation is essential. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.012DOI Listing

HDAC inhibition induces autophagy and mitochondrial biogenesis to maintain mitochondrial homeostasis during cardiac ischemia/reperfusion injury.

J Mol Cell Cardiol 2019 Mar 14;130:36-48. Epub 2019 Mar 14.

Dept. of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, AL 35233, United States of America. Electronic address:

Aims: The FDA-approved histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA, Vorinostat) has been shown to induce cardiomyocyte autophagy and blunt ischemia/reperfusion (I/R) injury when administered at the time of reperfusion. However, the precise mechanisms underlying the cardioprotective activity of SAHA are unknown. Mitochondrial dysfunction and oxidative damage are major contributors to myocardial apoptosis during I/R injury. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.008DOI Listing
March 2019
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4.655 Impact Factor

MicroRNA-143-3p promotes human cardiac fibrosis via targeting sprouty3 after myocardial infarction.

J Mol Cell Cardiol 2019 Mar 14;129:281-292. Epub 2019 Mar 14.

Department of Pathology and Forensic Medicine, College of Basic Medical Sciences, Dalian Medical University, Dalian 116044, Liaoning Province, China. Electronic address:

Myocardial infarction (MI) is one of the most catastrophic diseases threatening human health in the world. Because cardiomyocytes have a minuscule regenerative potential, the natural repair of infarct healing after MI shows fibrotic scar. MicroRNA-143-3p (miR-143-3p) plays a critical regulatory role in various pathophysiological processes in the heart. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.005DOI Listing
March 2019
3 Reads
4.655 Impact Factor

Molecular and clinical implications of natriuretic peptides in aortic valve stenosis.

J Mol Cell Cardiol 2019 Mar 14;129:266-271. Epub 2019 Mar 14.

Department of Clinical and Molecular Medicine, School of Medicine and Psychology, Sapienza University of Rome, Italy; IRCCS Neuromed, Pozzilli (Isernia), Italy. Electronic address:

Aortic valve stenosis (AS) is the most common heart valve disease in North America and Europe leading to an increased risk of heart failure and death. A multidisciplinary evaluation of symptoms, individual risk profile, echocardiographic parameters, biomarkers assessment is required for an appropriate clinical and therapeutic management of AS. The natriuretic peptides (NPs) represent an important biomarker for diagnostic, prognostic and therapeutic purposes in several cardiovascular diseases. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.011DOI Listing
March 2019
2 Reads

Circular RNA Ttc3 regulates cardiac function after myocardial infarction by sponging miR-15b.

J Mol Cell Cardiol 2019 Mar 12;130:10-22. Epub 2019 Mar 12.

Department of Cardiology, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Hongkou District, Shanghai, China. Electronic address:

The apoptotic death of cardiomyocytes critically contributes to cardiac remodeling after myocardial infarction (MI). Circular RNAs (circRNAs) are important regulators for a variety of biological functions. Circ-Ttc3 represents one of the top highest expressed circRNAs in the heart; however, its role in MI remains unknown. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.007DOI Listing
March 2019
1 Read

Bicuspid aortic valve, atherosclerosis and changes of lipid metabolism: Are there pathological molecular links?

Authors:
Paolo Magni

J Mol Cell Cardiol 2019 Mar 11;129:231-235. Epub 2019 Mar 11.

Dipartimento di Scienze Farmacologiche e Biomolecolari, Universita' degli Studi di Milano, Via Balzaretti 9, 20133 Milano, Italy; IRCCS MultiMedica, via Milanese 300, 20099, Sesto S. Giovanni, Milano, Italy. Electronic address:

Bicuspid aortic valve (BAV) is recognized as a syndrome including aortic valve diseases and aortic wall alterations, such as aortic dilatation, dissection and rupture, but also coronary atherosclerosis. The current evidence, although partially controversial, suggests that several molecular mechanisms promoting atherosclerosis are activated in BAV patients and are involved in the progression of the related diseases, from aortic stenosis to aortopathies, along with altered hemodynamics. Among these factors, dyslipidemia (i. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.004DOI Listing

Ablation of the calpain-targeted site in cardiac myosin binding protein-C is cardioprotective during ischemia-reperfusion injury.

J Mol Cell Cardiol 2019 Mar 9;129:236-246. Epub 2019 Mar 9.

Department of Cell and Molecular Physiology, Loyola University Chicago, Maywood, IL, USA; Heart, Lung and Vascular Institute, Division of Cardiovascular Health and Disease, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA. Electronic address:

Cardiac myosin binding protein-C (cMyBP-C) phosphorylation is essential for normal heart function and protects the heart from ischemia-reperfusion (I/R) injury. It is known that protein kinase-A (PKA)-mediated phosphorylation of cMyBP-C prevents I/R-dependent proteolysis, whereas dephosphorylation of cMyBP-C at PKA sites correlates with its degradation. While sites on cMyBP-C associated with phosphorylation and proteolysis co-localize, the mechanisms that link cMyBP-C phosphorylation and proteolysis during cardioprotection are not well understood. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.006DOI Listing
March 2019
2 Reads

Mir-455-3p-1 represses FGF7 expression to inhibit pulmonary arterial hypertension through inhibiting the RAS/ERK signaling pathway.

J Mol Cell Cardiol 2019 Mar 8;130:23-35. Epub 2019 Mar 8.

Department of Anesthesiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100037, China. Electronic address:

Objective: To analyze the effects of miR-455-3p-1 and its possible mechanisms in pulmonary arterial hypertension (PAH).

Methods: A microarray assay was used to examine the expressed genes between normal and PAH. The expressed genes in PAH was assessed by qRT-PCR. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.002DOI Listing

What to do with repeated measurements of a continuous response variable.

Authors:
Rachel Nordgren

J Mol Cell Cardiol 2019 Mar 7. Epub 2019 Mar 7.

Institute for Health and Research Policy, School of Public Health, University of Illinois at Chicago, Chicago, IL, United States of America. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.001DOI Listing

Activation of the cation channel TRPM3 in perivascular nerves induces vasodilation of resistance arteries.

J Mol Cell Cardiol 2019 Mar 7;129:219-230. Epub 2019 Mar 7.

Department of Cellular and Molecular Medicine, Laboratory of Ion Channel Research, KU Leuven, VIB Center for Brain & Disease Research, Herestraat 49, Campus Gasthuisberg, O&N1 Box 802, 3000 Leuven, Belgium. Electronic address:

The Transient Receptor Potential Melastatin 3 (TRPM3) is a Ca-permeable non-selective cation channel activated by the neurosteroid pregnenolone sulfate (PS). This compound was previously shown to contract mouse aorta by activating TRPM3 in vascular smooth muscle cells (VSMC), and proposed as therapeutic modulator of vascular functions. However, PS effects and the role of TRPM3 in resistance arteries remain unknown. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.03.003DOI Listing

Cytoplasmic nucleic acid-based XNAs directly enhance live cardiac cell function by a Ca cycling-independent mechanism via the sarcomere.

J Mol Cell Cardiol 2019 Mar 5;130:1-9. Epub 2019 Mar 5.

Department of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, United States of America. Electronic address:

Nucleic acid - protein interactions are critical for regulating gene activation in the nucleus. In the cytoplasm, however, potential nucleic acid-protein functional interactions are less clear. The emergence of a large and expanding number of non-coding RNAs and DNA fragments raises the possibility that the cytoplasmic nucleic acids may interact with cytoplasmic cellular components to directly alter key biological processes within the cell. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.016DOI Listing
March 2019
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4.655 Impact Factor

Calculating a sample size for a study with repeated measures.

Authors:
Rachel Nordgren

J Mol Cell Cardiol 2019 Mar 4. Epub 2019 Mar 4.

Institute for Health and Research Policy, School of Public Health, University of Illinois at Chicago, Chicago, IL, United States of America. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.004DOI Listing

Myofilament Ca sensitivity correlates with left ventricular contractility during the progression of pressure overload-induced left ventricular myocardial hypertrophy in rats.

J Mol Cell Cardiol 2019 Mar 4;129:208-218. Epub 2019 Mar 4.

Heart and Vascular Center, Semmelweis University, Budapest, Hungary.

Aim: Here we aimed at investigating the relation between left ventricular (LV) contractility and myofilament function during the development and progression of pressure overload (PO)-induced LV myocardial hypertrophy (LVH).

Methods: Abdominal aortic banding (AB) was performed to induce PO in rats for 6, 12 and 18 weeks. Sham operated animals served as controls. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.017DOI Listing

Multiple roles of KLF15 in the heart: Underlying mechanisms and therapeutic implications.

J Mol Cell Cardiol 2019 Mar 2;129:193-196. Epub 2019 Mar 2.

Pediatric Research Institute, Departments of Pediatrics, Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Louisville, KY 40292, USA. Electronic address:

Although there is an increasing understanding of the signaling pathways that promote cardiac hypertrophy, negative regulatory factors of this process have received less attention. Increasing evidence indicates that Krüppel-like factor 15 (KLF15) plays an important role in maintaining cardiac function by controlling the transcriptional pathways that regulating cardiac metabolism. Recent studies have also revealed a vital role for KLF15 as an inhibitor of pathological cardiac hypertrophy and fibrosis via its effects on factors such as myocyte enhancer factor 2 (MEF2), GATA-binding protein 4 (GATA4), transforming growth factor-β (TGF-β), and myocardin. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.024DOI Listing
March 2019
4 Reads
4.655 Impact Factor

New imaging techniques project the cellular and molecular alterations underlying bicuspid aortic valve development.

J Mol Cell Cardiol 2019 Mar 1;129:197-207. Epub 2019 Mar 1.

Department of Cardiothoracic Sciences, University of Campania "L. Vanvitelli", Naples, Italy.

Bicuspid aortic valve (BAV) disease is the most common congenital cardiac malformation associated with an increased lifetime risk and a high rate of surgically-relevant valve deterioration and aortic dilatation. Genomic data revealed that different genes are associated with BAV. A dominant genetic factor for the recent past was the basis to the recommendation for a more extensive aortic intervention. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.015DOI Listing

HDAC inhibition as a therapeutic strategy in myocardial ischemia/reperfusion injury.

J Mol Cell Cardiol 2019 Feb 27;129:188-192. Epub 2019 Feb 27.

Department of Internal Medicine, Division of Cardiology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America; Department of Molecular Biology, UT Southwestern Medical Center, 6000 Harry Hines Blvd. NB11.200, Dallas, United States of America.

Reperfusion injury during myocardial infarction accounts for approximately half of final infarct size. Whereas this has been known for decades, efficacious therapy targeting reperfusion injury remains elusive. Many proteins are subject to reversible acetylation, and drugs targeting enzymes that govern these events have emerged in oncology. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.013DOI Listing
February 2019

Polyamines and microbiota in bicuspid and tricuspid aortic valve aortopathy.

J Mol Cell Cardiol 2019 Feb 28;129:179-187. Epub 2019 Feb 28.

Department of Experimental Medical Science, Lund University, Lund, Sweden. Electronic address:

Polyamines are small aliphatic cationic molecules synthesized via a highly regulated pathway and involved in general molecular and cellular phenomena. Both mammalian cells and microorganisms synthesize polyamines, and both sources may contribute to the presence of polyamines in the circulation. The dominant location for microorganisms within the body is the gut. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.014DOI Listing
February 2019
1 Read

Adropin treatment restores cardiac glucose oxidation in pre-diabetic obese mice.

J Mol Cell Cardiol 2019 Feb 26;129:174-178. Epub 2019 Feb 26.

Division of Cardiology, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA; Center for Metabolism and Mitochondrial Medicine, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address:

Exposure to a high fat (HF) diet promotes increased fatty acid uptake, fatty acid oxidation and lipid accumulation in the heart. These maladaptive changes impact cellular energy metabolism and may promote the development of cardiac dysfunction. Attempts to increase cardiac glucose utilization have been proposed as a way to reverse cardiomyopathy in obese and diabetic individuals. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.012DOI Listing
February 2019
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Paraoxonase 2 protects against acute myocardial ischemia-reperfusion injury by modulating mitochondrial function and oxidative stress via the PI3K/Akt/GSK-3β RISK pathway.

J Mol Cell Cardiol 2019 Feb 23;129:154-164. Epub 2019 Feb 23.

Department of Medicine, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, United States of America; Molecular Toxicology Interdepartmental Degree Program, University of California, Los Angeles, United States of America. Electronic address:

Objective: To investigate the novel role of Paraoxonase 2 (PON2) in modulating acute myocardial ischemia-reperfusion injury (IRI).

Approach: IRI was induced both in vivo and ex vivo in male, C57BL6/J (WT) and PON2-deficient (PON-def) mice. In addition, in vitro hypoxia-reoxygenation injury (HRI) was induced in H9c2 cells expressing empty vector (H9c2-EV) or human PON2 (H9c2-hPON2) ± LY294002 (a potent PI3K inhibitor). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.008DOI Listing
February 2019
3 Reads

Overexpression of inducible nitric oxide synthase in the diabetic heart compromises ischemic postconditioning.

J Mol Cell Cardiol 2019 Feb 21;129:144-153. Epub 2019 Feb 21.

Division of Cardiac Surgery, Heart center, The First Affiliated Hospital, Sun Yat-sen University, China; NHC Key Laboratory of Assisted Circulation, Sun Yat-sen University, PR China; National and Guangdong Province Joint Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases, PR China; Guangdong Provincial Key Laboratory of Brain Function and Disease, Guangzhou 510080, PR China. Electronic address:

Ischemia postconditioning (PTC) can reduce myocardial ischemia/reperfusion injury. However, the effectiveness of PTC cardioprotection is reduced or lost in diabetes and the mechanisms are largely unclear. Hyperglycemia can induce overexpression of inducible nitric oxide synthesis (iNOS) in the myocardium of diabetic subjects. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.011DOI Listing
February 2019
3 Reads
4.655 Impact Factor