8,171 results match your criteria Journal of molecular and cellular cardiology[Journal]


The cardiomyocyte "redox rheostat": Redox signalling via the AMPK-mTOR axis and regulation of gene and protein expression balancing survival and death.

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

School of Biological Sciences, University of Reading, Whiteknights, Reading RG6 6AS, UK; National Heart and Lung Institute (Cardiovascular Sciences), Faculty of Medicine, Flowers Building, Imperial College, SW7 2AZ, UK and Dovehouse Street, London SW3 6LY, UK.

Reactive oxygen species (ROS) play a key role in development of heart failure but, at a cellular level, their effects range from cytoprotection to induction of cell death. Understanding how this is regulated is crucial to develop novel strategies to ameliorate only the detrimental effects. Here, we revisited the fundamental hypothesis that the level of ROS per se is a key factor in the cellular response by applying different concentrations of HO to cardiomyocytes. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.006DOI Listing
February 2019

Pre-existing fibroblasts of epicardial origin are the primary source of pathological fibrosis in cardiac ischemia and aging.

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

Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA; Department of Biomedical Engineering, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA; Department of Pharmacology and Physiology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA; Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Electronic address:

Serum response factor (SRF) and the SRF co-activators myocardin-related transcription factors (MRTFs) are essential for epicardium-derived progenitor cell (EPDC)-mobilization during heart development; however, the impact of developmental EPDC deficiencies on adult cardiac physiology has not been evaluated. Here, we utilize the Wilms Tumor-1 (Wt1)-Cre to delete Mrtfs or Srf in the epicardium, which reduced the number of EPDCs in the adult cardiac interstitium. Deficiencies in Wt1-lineage EPDCs prevented the development of cardiac fibrosis and diastolic dysfunction in aged mice. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.015DOI Listing
February 2019

Role of the PRC2-Six1-miR-25 signaling axis in heart failure.

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

Cardiovascular Research Center, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:

The reduced expression of cardiac sarco-endoplasmic reticulum Ca ATPase (SERCA2a) is a hallmark of heart failure. We previously showed that miR-25 is a crucial transcriptional regulator of SERCA2a in the heart. However, the precise mechanism of cardiac miR-25 regulation is largely unknown. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.017DOI Listing
February 2019

SPRED2 deficiency elicits cardiac arrhythmias and premature death via impaired autophagy.

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

Institute of Physiology, University of Wuerzburg, Germany. Electronic address:

Cardiac functionality is dependent on a balanced protein turnover. Accordingly, regulated protein decay is critical to maintain cardiac function. Here we demonstrate that deficiency of SPRED2, an intracellular repressor of ERK-MAPK signaling markedly expressed in human heart, resulted in impaired autophagy, heart failure, and shortened lifespan. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.023DOI Listing
February 2019

Regulation of cardiac transcription by thyroid hormone and Med13.

J Mol Cell Cardiol 2019 Feb 12. Epub 2019 Feb 12.

Department of Internal Medicine, Division of Cardiovascular Medicine, Francois M. Abboud Cardiovascular Research Center, Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA. Electronic address:

Thyroid hormone (TH) is a key regulator of transcriptional homeostasis in the heart. While hypothyroidism is known to result in adverse cardiac effects, the molecular mechanisms that modulate TH signaling are not completely understood. Mediator is a multiprotein complex that coordinates signal-dependent transcription factors with the basal transcriptional machinery to regulate gene expression. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.007DOI Listing
February 2019

Activation of the calcium-sensing receptor in human valvular interstitial cells promotes calcification.

J Mol Cell Cardiol 2019 Feb 12. Epub 2019 Feb 12.

EA7517, MP3CV, CURS, University of Picardie Jules Verne, Amiens, France; Biochemistry Laboratory, Amiens University Hospital, Amiens, France. Electronic address:

Introduction And Aims: Calcific aortic valve disease (CAVD) is the most common heart valve disease in western countries. It has been reported that activation of the calcium-sensing receptor(CaSR) expressed by vascular smooth muscle cells prevents vascular calcification. However, to date, the CaSR's expression and function in cardiac valves have not been studied. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.021DOI Listing
February 2019

Mitochondrial MTG1 is necessary for proper human cardiomyocyte activity and zebrafish cardiac development. Comment to "Novel role of mitochondrial GTPases 1 in pathological cardiac hypertrophy".

J Mol Cell Cardiol 2019 Feb 11. Epub 2019 Feb 11.

Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL 33136, United States; Department of Neurology, University of Miami Miller School of Medicine, Miami, FL 33136, United States. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.005DOI Listing
February 2019
1 Read

Dysregulation of IL-33/ST2 signaling and myocardial periarteriolar fibrosis.

J Mol Cell Cardiol 2019 Feb 11. Epub 2019 Feb 11.

Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, 7 Divinity Ave, Cambridge, MA 02138, United States of America; Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 75 Francis St, Boston, MA 02115, United States of America. Electronic address:

Microvascular dysfunction in the heart and its association with periarteriolar fibrosis may contribute to the diastolic dysfunction seen in heart failure with preserved ejection fraction. Interleukin-33 (IL-33) prevents global myocardial fibrosis in a pressure overloaded left ventricle by acting via its receptor, ST2 (encoded by the gene, Il1rl1); however, whether this cytokine can also modulate periarteriolar fibrosis remains unclear. We utilized two approaches to explore the role of IL-33/ST2 in periarteriolar fibrosis. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.018DOI Listing
February 2019

PKC and PKN in heart disease.

J Mol Cell Cardiol 2019 Feb 8. Epub 2019 Feb 8.

Division of Cardiology, School of Medicine, University of California-San Diego, La Jolla, USA; University of Gothenburg, Wallenberg Laboratory, Department of Molecular and Clinical Medicine, Institute of Medicine, Gothenburg, Sweden. Electronic address:

The protein kinase C (PKC) and closely related protein kinase N (PKN) families of serine/threonine protein kinases play crucial cellular roles. Both kinases belong to the AGC subfamily of protein kinases that also include the cAMP dependent protein kinase (PKA), protein kinase B (PKB/AKT), protein kinase G (PKG) and the ribosomal protein S6 kinase (S6K). Involvement of PKC family members in heart disease has been well documented over the years, as their activity and levels are mis-regulated in several pathological heart conditions, such as ischemia, diabetic cardiomyopathy, as well as hypertrophic or dilated cardiomyopathy. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.029DOI Listing
February 2019
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Direct visualization of cardiac transcription factories reveals regulatory principles of nuclear architecture during pathological remodeling.

J Mol Cell Cardiol 2019 Feb 8. Epub 2019 Feb 8.

Departments of Anesthesiology, Medicine/Cardiology, Physiology, David Geffen School of Medicine at UCLA, 650 Charles Young Dr., Los Angeles, CA 90095, United States. Electronic address:

Heart failure is associated with hypertrophying of cardiomyocytes and changes in transcriptional activity. Studies from rapidly dividing cells in culture have suggested that transcription may be compartmentalized into factories within the nucleus, but this phenomenon has not been tested in vivo and the role of nuclear architecture in cardiac gene regulation is unknown. While alterations to transcription have been linked to disease, little is known about the regulation of the spatial organization of transcription and its properties in the pathological setting. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.003DOI Listing
February 2019

Stromal cell-derived factor-1α signals via the endothelium to protect the heart against ischaemia-reperfusion injury.

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

The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London WC1E 6HX, UK.

Aims: The chemokine stromal derived factor-1α (SDF-1α) is known to protect the heart acutely from ischaemia-reperfusion injury via its cognate receptor, CXCR4. However, the timing and cellular location of this effect, remains controversial.

Methods And Results: Wild type male and female mice were subjected to 40 min LAD territory ischaemia in vivo and injected with either saline (control) or SDF-1α prior to 2 h reperfusion. 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.2019.02.002DOI Listing
February 2019
5 Reads

Na microdomains and sparks: Role in cardiac excitation-contraction coupling and arrhythmias in ankyrin-B deficiency.

J Mol Cell Cardiol 2019 Feb 5;128:145-157. Epub 2019 Feb 5.

Department of Biomedical Engineering and the Institute for Computational Medicine, The Johns Hopkins University School of Medicine and Whiting School of Engineering, 3400 N Charles Street, Baltimore, MD 21218, USA. Electronic address:

Cardiac sodium (Na) potassium ATPase (NaK) pumps, neuronal sodium channels (I), and sodium calcium (Ca) exchangers (NCX1) may co-localize to form a Na microdomain. It remains controversial as to whether neuronal I contributes to local Na accumulation, resulting in reversal of nearby NCX1 and influx of Ca into the cell. Therefore, there has been great interest in the possible roles of a Na microdomain in cardiac Ca-induced Ca release (CICR). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.02.001DOI Listing
February 2019

Dedicator of cytokinesis 2 silencing therapy inhibits neointima formation and improves blood flow in rat vein grafts.

J Mol Cell Cardiol 2019 Feb 1;128:134-144. Epub 2019 Feb 1.

Department of Cardiothoracic Surgery, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University, Shanghai 200233, China. Electronic address:

Objective: The high rate of vein graft failure due to neointimal hyperplasia is a major challenge for cardiovascular surgery. Finding novel approaches to prevent neointimal hyperplasia is important. Thus, the purpose of this study was to investigate whether dedicator of cytokinesis 2 (DOCK2) plays a role in the development of neointima formation in the vein grafts. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.030DOI Listing
February 2019
1 Read

The protective effect of high mobility group protein HMGA2 in pressure overload-induced cardiac remodeling.

J Mol Cell Cardiol 2019 Jan 31;128:160-178. Epub 2019 Jan 31.

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, PR China; Hubei Key Laboratory of Cardiology, Wuhan 430060, PR China. Electronic address:

High mobility group protein AT-hook 2 (HMGA2), an architectural transcription factor, has previously been reported to play an essential role in regulating the expression of many genes through architectural remodeling processes. However, the effects of HMGA2 on cardiovascular disease, especial cardiac remodeling, is unclear. This study was aimed at investigating the functional role of HMGA2 in pressure overload-induced cardiac remodeling. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.027DOI Listing
January 2019

Double deletion of calponin 1 and calponin 2 in mice decreases systemic blood pressure with blunted length-tension response of aortic smooth muscle.

J Mol Cell Cardiol 2019 Jan 29. Epub 2019 Jan 29.

Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA. Electronic address:

Calponin is a family of actin filament-associated regulatory proteins. Among its three isoforms, calponin 1 is smooth muscle specific and calponin 2 is expressed in smooth muscle and certain non-muscle cells. Previous studies showed that calponin 1 knockout mice had detectable changes in the contractility of urogenital smooth muscle whereas other smooth muscles were less affected. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.026DOI Listing
January 2019
2 Reads

Novel role of mitochondrial GTPases 1 in pathological cardiac hypertrophy.

J Mol Cell Cardiol 2019 Jan 29;128:105-116. Epub 2019 Jan 29.

Department of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. Electronic address:

While most mitochondrial proteins are encoded in the nucleus and translated on cytosolic/endoplasmic reticulum ribosomes, proteins encoded by mitochondrial DNA are translated on mitochondrial ribosomes. Mitochondrial GTPases 1 (MTG1) regulates mitochondrial ribosome assembly and translation, but its impact on cardiac adaptation to stress is unknown. Here, we found that MTG1 is dramatically elevated in hearts of dilated cardiomyopathy patients and in mice exposed to left ventricular pressure overload (AB). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.025DOI Listing
January 2019
2 Reads
4.655 Impact Factor

The more we learn, the less we know: A novel cardiac mechanism of brain damage.

J Mol Cell Cardiol 2019 Jan 28;128:158-159. Epub 2019 Jan 28.

Department of Medicine, Medical University of South Carolina, Charleston, SC, United States. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.016DOI Listing
January 2019

Cardiac repair and the putative role of stem cells.

J Mol Cell Cardiol 2019 Jan 28;128:96-104. Epub 2019 Jan 28.

Department of Pathology and Laboratory Medicine, McGovern Medical School, Houston, TX, USA; The University of Texas Health Science Center at Houston (UTHealth), Houston, TX, USA; Cardiovascular Pathology Laboratory, Texas Heart Institute, St. Luke's Episcopal Hospital, Houston, TX, USA. Electronic address:

Stem cell biology has informed and energized cardiac regenerative medicine. The field is linked to a construct that challenges long-standing concepts and advances the basic tenets that: 1) the mammalian heart has the capacity for significant regeneration of cardiomyocytes (CMC) by reentry of CMC into the cell cycle and by activation of endogenous cardiac stem cells and 2) the administration of exogenous stem cell preparations can result in significant myocardial repair and regeneration in cardiac diseases. Based on the latter, major resources have been invested in clinical trials of stem cell therapy. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.022DOI Listing
January 2019

Epigenetics, cardiovascular disease, and cellular reprogramming.

J Mol Cell Cardiol 2019 Jan 25;128:129-133. Epub 2019 Jan 25.

Department of Diabetes, Epigenetics in Human Health and Disease Laboratory, Monash University, Melbourne, VIC, Australia; Hong Kong Institute of Diabetes and Obesity, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Region.

Under the seeming disorder of "junk" sequences the last decade has seen developments in our understanding of non-coding RNA's (ncRNAs). It's a complex revised order and nowhere is this more relevant than in the developing heart whereby old rules have been set aside to make room for new ones. The development of the mammalian heart has been studied at the genetic and cellular level for several decades because these areas were considered ideal control points. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.019DOI Listing
January 2019

Characterization of a small molecule that promotes cell cycle activation of human induced pluripotent stem cell-derived cardiomyocytes.

J Mol Cell Cardiol 2019 Jan 23;128:90-95. Epub 2019 Jan 23.

Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. Electronic address:

Background: Since regenerative capacity of adult mammalian myocardium is limited, activation of the endogenous proliferative capacity of existing cardiomyocytes is a potential therapeutic strategy for treating heart diseases accompanied by cardiomyocyte loss. Recently, we performed a compound screening and developed a new drug named TT-10 (CHFNOS) which promotes the proliferation of murine cardiomyocytes via enhancement of YES-associated protein (YAP)-transcriptional enhancer factor domain (TEAD) activity and improves cardiac function after myocardial infarction in adult mice.

Methods And Results: To test whether TT-10 can also promote the proliferative capacity of human cardiomyocytes, we investigated the efficacy of TT-10 on human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes (hiPSCMs). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.020DOI Listing
January 2019
1 Read

New insights on the cardiac safety factor: Unraveling the relationship between conduction velocity and robustness of propagation.

J Mol Cell Cardiol 2019 Jan 22;128:117-128. Epub 2019 Jan 22.

IHU Liryc, Electrophysiology and Heart Modeling Institute, Pessac-Bordeaux, France; Université de Bordeaux, Talence, France. Electronic address:

Cardiac conduction disturbances are linked with arrhythmia development. The concept of safety factor (SF) has been derived to describe the robustness of conduction, but the usefulness of this metric has been constrained by several limitations. For example, due to the difficulty of measuring the necessary input variables, SF calculations have only been applied to synthetic data. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.010DOI Listing
January 2019
2 Reads

Acute ATR blockade prevents isoproterenol-induced injury in mdx hearts.

J Mol Cell Cardiol 2019 Jan 19;128:51-61. Epub 2019 Jan 19.

Department of Integrative Biology and Physiology, University of Minnesota Medical School, Minneapolis, MN, USA; Lillehei Heart Institute, University of Minnesota Medical School, Minneapolis, MN, USA. Electronic address:

Background: Duchenne muscular dystrophy (DMD) is an X-linked disease characterized by skeletal muscle degeneration and a significant cardiomyopathy secondary to cardiomyocyte damage and myocardial loss. The molecular basis of DMD lies in the absence of the protein dystrophin, which plays critical roles in mechanical membrane integrity and protein localization at the sarcolemma. A popular mouse model of DMD is the mdx mouse, which lacks dystrophin and displays mild cardiac and skeletal pathology that can be exacerbated to advance the disease state. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183126
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http://dx.doi.org/10.1016/j.yjmcc.2019.01.013DOI Listing
January 2019
3 Reads

Regulation of DNA methylation and 2-OG/TET signaling by choline alleviated cardiac hypertrophy in spontaneously hypertensive rats.

J Mol Cell Cardiol 2019 Jan 17;128:26-37. Epub 2019 Jan 17.

Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, PR China. Electronic address:

DNA methylation is a well-defined epigenetic modification that regulates gene transcription. However, the role of DNA methylation in the cardiac hypertrophy seen in hypertension is unclear. This study was performed to investigate genome-wide DNA methylation profiles in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats (WKY), and the cardioprotective effect of choline. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.011DOI Listing
January 2019
1 Read

Corrigendum to increased expression of DRAM1 confers myocardial protection against ischemia via restoring autophagy flux [J Mol Cell Cardiol. 2018 Nov;124:70-82].

J Mol Cell Cardiol 2019 Feb 16;127:277. Epub 2019 Jan 16.

Key Laboratory of Molecular Clinical Pharmacology & Fifth Affiliated Hospital, Guangzhou Medical University. Guangzhou, Guangdong 511436, PR China; Guangzhou Institute of Cardiovascular Disease, Guangzhou Key Laboratory of Cardiovascular Disease & The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, PR China. Electronic address:

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183130
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http://dx.doi.org/10.1016/j.yjmcc.2018.12.009DOI Listing
February 2019
3 Reads

DNA methyltransferase 1 and Krüppel-like factor 4 axis regulates macrophage inflammation and atherosclerosis.

J Mol Cell Cardiol 2019 Jan 16;128:11-24. Epub 2019 Jan 16.

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100191, PR China. Electronic address:

Macrophage-mediated inflammatory responses occur throughout all stages of atherosclerosis. DNA methylation is one of the critical epigenetic mechanisms and is associated with the development of atherosclerosis. The underlying mechanism of epigenetic regulation of macrophage inflammation (M1 activation) remains unclear. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.009DOI Listing
January 2019
1 Read

Prenatal exposure to testosterone induces cardiac hypertrophy in adult female rats through enhanced Pkcδ expression in cardiac myocytes.

J Mol Cell Cardiol 2019 Jan 11;128:1-10. Epub 2019 Jan 11.

Department of Reproductive Medicine, International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University, Shanghai 200030, China; Institute of Embryo-Fetal Original Adult Disease, School of Medicine, Shanghai Jiao Tong University, Shanghai 200030,China. Electronic address:

High circulating androgen in women with polycystic ovary syndrome (PCOS) may increase the risk of cardiovascular disease in offspring. The aim of the present study is to investigate whether maternal androgen excess in the rat PCOS model would lead to cardiac hypertrophy in offspring. Maternal testosterone propionate (maternal-TP)-treated adult female offspring displayed cardiac hypertrophy associated with local high cardiac dihydrotestosterone (DHT). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.008DOI Listing
January 2019
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Recent advances in understanding the roles of T cells in pressure overload-induced cardiac hypertrophy and remodeling.

J Mol Cell Cardiol 2019 Jan 11. Epub 2019 Jan 11.

Department of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China. Electronic address:

Pressure overload-induced cardiac hypertrophy and remodeling are not simply mechanical responses to overloaded stress. They also involve participation of various immune cells, especially T cells. In this review, we summarized recent advances in understanding the roles of T cells in this process and the possible mechanisms underlying T cells involvement and modulation. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.005DOI Listing
January 2019
1 Read
4.655 Impact Factor

Inhibition of LPS-stimulated ecto-adenosine deaminase attenuates endothelial cell activation.

J Mol Cell Cardiol 2019 Jan 11;128:62-76. Epub 2019 Jan 11.

Department of Biochemistry, Medical University of Gdansk, 1 Debinki St., 80-211 Gdansk, Poland. Electronic address:

Vascular inflammation is an important factor in the pathophysiology of cardiovascular diseases, such as atherosclerosis. Changes in the extracellular nucleotide and in particular adenosine catabolism may alter a chronic inflammation and endothelial activation. This study aimed to evaluate the relation between vascular ecto-adenosine deaminase (eADA) activity and endothelial activation in humans and to analyze the effects of LPS-mediated inflammation on this activity as well as mechanisms of its increase. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.004DOI Listing
January 2019
1 Read

Power analysis and sample size calculation.

J Mol Cell Cardiol 2019 Jan 11. Epub 2019 Jan 11.

Center for Biostatistics, Department of Population Health Science and Policy, Icahn School of Medicine at Mount Sinai, New York, NY, United States.

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.006DOI Listing
January 2019

Macrophage fatty acid oxidation inhibits atherosclerosis progression.

J Mol Cell Cardiol 2019 Feb 9;127:270-276. Epub 2019 Jan 9.

Center for Molecular Medicine, NIH, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA; Aging Institute, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA. Electronic address:

Atherosclerosis is a chronic disorder of the vessel wall. One key regulator of disease progression is lipid handling in macrophages. However, the role of macrophage mitochondrial-dependent fatty acid β-oxidation (FAO) in atherosclerosis is not well defined. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.003DOI Listing
February 2019
1 Read

CaMKII signaling in heart diseases: Emerging role in diabetic cardiomyopathy.

J Mol Cell Cardiol 2019 Feb 8;127:246-259. Epub 2019 Jan 8.

Department of Pharmacology, University of California Davis, Davis, CA, USA.

Calcium/calmodulin-dependent protein kinase II (CaMKII) is upregulated in diabetes and significantly contributes to cardiac remodeling with increased risk of cardiac arrhythmias. Diabetes is frequently associated with atrial fibrillation, coronary artery disease, and heart failure, which may further enhance CaMKII. Activation of CaMKII occurs downstream of neurohormonal stimulation (e. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2019.01.001DOI Listing
February 2019
1 Read

Circulating CD14CD16 classical monocytes do not associate with a vulnerable plaque phenotype, and do not predict secondary events in severe atherosclerotic patients.

J Mol Cell Cardiol 2019 Feb 7;127:260-269. Epub 2019 Jan 7.

Laboratory for Experimental Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands.; Laboratory of Translational Immunology, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address:

Aims: Mouse studies have established distinct monocyte subtypes that participate in the process of atherosclerotic lesion formation. The pro-inflammatory Ly6C monocyte subtype actively contributes to murine plaque progression and destabilization. Also in humans, different peripheral monocyte subtypes have been identified, of which the CD14CD16 classical monocyte is suggested to display similar pro-atherosclerotic properties as the murine Ly6C subtype. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828193001
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http://dx.doi.org/10.1016/j.yjmcc.2019.01.002DOI Listing
February 2019
3 Reads
4.655 Impact Factor

Mitochondrial LonP1 protects cardiomyocytes from ischemia/reperfusion injury in vivo.

J Mol Cell Cardiol 2019 Jan 6;128:38-50. Epub 2019 Jan 6.

Department of Microbiology, Biochemistry & Molecular Genetics, New Jersey Medical School- Rutgers, The State University of New Jersey, Newark, NJ, USA. Electronic address:

Rationale: LonP1 is an essential mitochondrial protease, which is crucial for maintaining mitochondrial proteostasis and mitigating cell stress. However, the importance of LonP1 during cardiac stress is largely unknown.

Objective: To determine the functions of LonP1 during ischemia/reperfusion (I/R) injury in vivo, and hypoxia-reoxygenation (H/R) stress in vitro. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.017DOI Listing
January 2019
2 Reads

Cardiac-specific deficiency of the mitochondrial calcium uniporter augments fatty acid oxidation and functional reserve.

J Mol Cell Cardiol 2019 Feb 4;127:223-231. Epub 2019 Jan 4.

Cardiovascular Translational Science Institute and the Department of Pediatrics, 423 Heritage Medical Research Building, University of Alberta, Edmonton, Alberta T6G 2S2, Canada. Electronic address:

The mitochondrial calcium uniporter (MCU) relays cytosolic Ca transients to the mitochondria. We examined whether energy metabolism was compromised in hearts from mice with a cardiac-specific deficiency of MCU subjected to an isoproterenol (ISO) challenge. Surprisingly, isolated working hearts from cardiac MCU-deficient mice showed higher cardiac work, both in the presence or absence of ISO. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.019DOI Listing
February 2019

Chemically synthesized Secoisolariciresinol diglucoside (LGM2605) improves mitochondrial function in cardiac myocytes and alleviates septic cardiomyopathy.

J Mol Cell Cardiol 2019 Feb 3;127:232-245. Epub 2019 Jan 3.

Center for Translational Medicine and Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA. Electronic address:

Sepsis is the overwhelming systemic immune response to infection, which can result in multiple organ dysfunction and septic shock. Myocardial dysfunction during sepsis is associated with advanced disease and significantly increased in-hospital mortality. Our group has shown that energetic failure and excess reactive oxygen species (ROS) generation constitute major components of myocardial dysfunction in sepsis. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359996PMC
February 2019
2 Reads

High-throughput single-molecule RNA imaging analysis reveals heterogeneous responses of cardiomyocytes to hemodynamic overload.

J Mol Cell Cardiol 2019 Jan 3;128:77-89. Epub 2019 Jan 3.

Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address:

Background: The heart responds to hemodynamic overload through cardiac hypertrophy and activation of the fetal gene program. However, these changes have not been thoroughly examined in individual cardiomyocytes, and the relation between cardiomyocyte size and fetal gene expression remains elusive. We established a method of high-throughput single-molecule RNA imaging analysis of in vivo cardiomyocytes and determined spatial and temporal changes during the development of heart failure. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.018DOI Listing
January 2019
1 Read

Brain renin-angiotensin system blockade with orally active aminopeptidase A inhibitor prevents cardiac dysfunction after myocardial infarction in mice.

J Mol Cell Cardiol 2019 Feb 30;127:215-222. Epub 2018 Dec 30.

Laboratory of Central Neuropeptides in the Regulation of Body Fluid Homeostasis and Cardiovascular Functions, Collège de France, Center for Interdisciplinary Research in Biology (CIRB), INSERM U1050/CNRS UMR7241, 11 place Marcelin Berthelot, Paris 75005, France. Electronic address:

Brain renin-angiotensin system (RAS) hyperactivity has been implicated in sympathetic hyperactivity and progressive left ventricular (LV) dysfunction after myocardial infarction (MI). Angiotensin III, generated by aminopeptidase A (APA), is one of the main effector peptides of the brain RAS in the control of cardiac function. We hypothesized that orally administered firibastat (previously named RB150), an APA inhibitor prodrug, would attenuate heart failure (HF) development after MI in mice, by blocking brain RAS hyperactivity. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.008DOI Listing
February 2019
6 Reads

High-content phenotypic assay for proliferation of human iPSC-derived cardiomyocytes identifies L-type calcium channels as targets.

J Mol Cell Cardiol 2019 Feb 28;127:204-214. Epub 2018 Dec 28.

Department of Biomedical Engineering and Robert M. Berne Cardiovascular Research Center, University of Virginia, USA. Electronic address:

Over 5 million people in the United States suffer from heart failure, due to the limited ability to regenerate functional cardiac tissue. One potential therapeutic strategy is to enhance proliferation of resident cardiomyocytes. However, phenotypic screening for therapeutic agents is challenged by the limited ability of conventional markers to discriminate between cardiomyocyte proliferation and endoreplication (e. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.015DOI Listing
February 2019

Heterotypic docking compatibility of human connexin37 with other vascular connexins.

J Mol Cell Cardiol 2019 Feb 27;127:194-203. Epub 2018 Dec 27.

Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada. Electronic address:

Human vascular connexins (Cx37, Cx40, Cx43, and Cx45) can form various types of gap junction channels to synchronize vasodilation/constriction to control local circulation. Most of our knowledge on heterotypic gap junctions of these vascular connexins was from studies on rodent connexins. In human vasculature, the same four homolog connexins exist, but whether these human connexins can form heterotypic GJs as those of rodents have not been fully studied. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.013DOI Listing
February 2019

Effects of temperature on transjunctional voltage-dependent gating kinetics in Cx45 and Cx40 gap junction channels.

J Mol Cell Cardiol 2019 Feb 27;127:185-193. Epub 2018 Dec 27.

Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada. Electronic address:

Gap junctions (GJs) are intercellular channels directly linking neighbouring cells and are dodecamers of connexins. In the human heart, connexin40 (Cx40), Cx43, and Cx45 are expressed in different regions of the heart forming GJs ensuring rapid propagation of action potentials in the myocardium. Two of these connexins, Cx40 and Cx45, formed functional GJs with prominent transjunctional voltage-dependent gating (V-gating), which can be a mechanism to down regulate coupling conductance (G). Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.014DOI Listing
February 2019

β-Catenin phosphorylation at Y654 and Y142 is crucial for high mobility group box-1 protein-induced pulmonary vascular hyperpermeability.

J Mol Cell Cardiol 2019 Feb 25;127:174-184. Epub 2018 Dec 25.

Department of Pathophysiology, Key Laboratory for Shock and Microcirculation Research of Guangdong Province, Guangdong Provincial Key Laboratory of Proteomics, State Key Laboratory of Organ Failure Research, Southern Medical University, Guangzhou 510515, China. Electronic address:

Objective: Endothelial hyperpermeability is a hallmark of acute lung injury in response to sepsis. The imbalance between adherence junction (AJ) mediated cell-cell adherence forces and stress fiber driven contractile forces contributes to increased endothelial permeability. Here, we spotlight the effects of β-catenin Y654 andY142 phosphorylation on HMGB1-mediated endothelial barrier leakage. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.012DOI Listing
February 2019
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Decreased α-tubulin acetylation induced by an acidic environment impairs autophagosome formation and leads to rat cardiomyocyte injury.

J Mol Cell Cardiol 2019 Feb 21;127:143-153. Epub 2018 Dec 21.

Institute of Burn Research, State Key Laboratory of Trauma, Burns and Combined Injury, Southwest Hospital, Third Military Medical University, Chongqing, China. Electronic address:

Extracellular pH strongly affects cellular metabolism and function. An acidic environment induced under pathological conditions leads to cardiomyocyte injury and dysfunction, but the underlying mechanisms are still poorly understood. Autophagy has been reported as a cytoprotective mechanism that maintains cellular metabolism and viability by removing misfolded proteins and damaged organelles. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.011DOI Listing
February 2019
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Heat-shock protein 90 modulates cardiac ventricular hypertrophy via activation of MAPK pathway.

J Mol Cell Cardiol 2019 Feb 22;127:134-142. Epub 2018 Dec 22.

Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 1920392, Japan. Electronic address:

The Raf/MAPK/ERK kinase (Mek)/extracellular signal-regulated kinases (Erk) pathway is activated in cardiac hypertrophy after a myocardial infarction. Although heat-shock protein 90 (Hsp90) may regulate the Raf/Mek/Erk signal pathway, the role of Hsp90 in pathophysiological cardiac hypertrophy remains unclear. In this study, we examined the role of Hsp90 in this pathway in cardiac hypertrophy under in vivo and in vitro experimental conditions. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183093
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http://dx.doi.org/10.1016/j.yjmcc.2018.12.010DOI Listing
February 2019
5 Reads

Corrigendum to "Aldehyde dehydrogenase 2 activation ameliorates cyclophosphamide-induced acute cardiotoxicity via detoxification of toxic aldehydes and suppression of cardiac cell death" [Journal of Molecular and Cellular Cardiology (JMCC) volume 121 (2018) 134-144].

J Mol Cell Cardiol 2019 Feb 19;127:115. Epub 2018 Dec 19.

Department of Emergency Medicine and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, China; Clinical Research Center for Emergency and Critical Care Medicine of Shandong Province, Institute of Emergency and Critical Care Medicine of Shandong University, Qilu Hospital of Shandong University, Jinan, China; Key Laboratory of Emergency and Critical Care Medicine of Shandong Province, Key Laboratory of Cardiopulmonary-Cerebral Resuscitation Research of Shandong Province, Qilu Hospital of Shandong University, Jinan, China; 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, China. Electronic address:

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http://dx.doi.org/10.1016/j.yjmcc.2018.10.019DOI Listing
February 2019
2 Reads

Cardiomyocyte cell cycle dynamics and proliferation revealed through cardiac-specific transgenesis of fluorescent ubiquitinated cell cycle indicator (FUCCI).

J Mol Cell Cardiol 2019 Feb 18;127:154-164. Epub 2018 Dec 18.

SDSU Heart Research Institute, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182, USA. Electronic address:

Rationale: Understanding and manipulating the cardiomyocyte cell cycle has been the focus of decades of research, however the ultimate goal of activating mitotic activity in adult mammalian cardiomyocytes remains elusive and controversial. The relentless pursuit of controlling cardiomyocyte mitosis has been complicated and obfuscated by a multitude of indices used as evidence of cardiomyocyte cell cycle activity that lack clear identification of cardiomyocyte "proliferation" versus cell cycle progression, endoreplication, endomitosis, and even DNA damage. Unambiguous appreciation of the complexity of cardiomyocyte replication that avoids oversimplification and misinterpretation is desperately needed. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183085
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http://dx.doi.org/10.1016/j.yjmcc.2018.12.007DOI Listing
February 2019
7 Reads

Atg2, Atg9 and Atg18 in mitochondrial integrity, cardiac function and healthspan in Drosophila.

J Mol Cell Cardiol 2019 Feb 17;127:116-124. Epub 2018 Dec 17.

Department of Medicine, University of Virginia, Charlottesville, VA 22908, United States; Department of Pharmacology, University of Virginia, Charlottesville, VA 22908, United States; Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA 22908, United States; Center for Skeletal Muscle Research at Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, United States. Electronic address:

In yeast, the Atg2-Atg18 complex regulates Atg9 recycling from phagophore assembly site during autophagy; their function in higher eukaryotes remains largely unknown. In a targeted screening in Drosophila melanogaster, we show that Mef2-GAL4-RNAi-mediated knockdown of Atg2, Atg9 or Atg18 in the heart and indirect flight muscles led to shortened healthspan (declined locomotive function) and lifespan. These flies displayed an accelerated age-dependent loss of cardiac function along with cardiac hypertrophy (increased heart tube wall thickness) and structural abnormality (distortion of the lumen surface). Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00222828183129
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http://dx.doi.org/10.1016/j.yjmcc.2018.12.006DOI Listing
February 2019
14 Reads

A long noncoding RNA NR_045363 controls cardiomyocyte proliferation and cardiac repair.

J Mol Cell Cardiol 2019 Feb 13;127:105-114. Epub 2018 Dec 13.

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

Long noncoding RNAs (lncRNAs) play important roles in the regulation of genes involved in cell proliferation. We have previously sought to more globally understand the differences of lncRNA expression between human fetal heart and adult heart to identify some functional lncRNAs which involve in the process of heart repair. We found that a highly conserved long noncoding RNA NR_045363 was mainly expressed in cardiomyocytes and rarely in non-cardiomyocytes. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.005DOI Listing
February 2019

Drp1/Fis1-mediated mitochondrial fragmentation leads to lysosomal dysfunction in cardiac models of Huntington's disease.

J Mol Cell Cardiol 2019 Feb 11;127:125-133. Epub 2018 Dec 11.

Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, United States. Electronic address:

Huntington's disease (HD) is a fatal hereditary neurodegenerative disorder, best known for its clinical triad of progressive motor impairment, cognitive deficits and psychiatric disturbances, is caused by CAG-repeat expansion in exon 1 of Huntingtin (HTT). However, in addition to the neurological disease, mutant HTT (mHTT), which is ubiquitously expressed in all tissues, impairs other organ systems. Not surprisingly, cardiovascular dysautonomia as well as the deterioration of circadian rhythms are among the earliest detectable pathophysiological changes in individuals with HD. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.004DOI Listing
February 2019
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MYBPC3 truncation mutations enhance actomyosin contractile mechanics in human hypertrophic cardiomyopathy.

J Mol Cell Cardiol 2019 Feb 11;127:165-173. Epub 2018 Dec 11.

Department of Molecular Physiology and Biophysics, Cardiovascular Research Institute of Vermont, University of Vermont, Burlington, VT, United States. Electronic address:

Rationale: Truncation mutations in the MYBPC3 gene, encoding for cardiac myosin-binding protein C (MyBP-C), are the leading cause of hypertrophic cardiomyopathy (HCM). Whole heart, fiber and molecular studies demonstrate that MyBP-C is a potent modulator of cardiac contractility, but how these mutations contribute to HCM is unresolved.

Objectives: To readdress whether MYBPC3 truncation mutations result in loss of MyBP-C content and/or the expression of truncated MyBP-C from the mutant allele and determine how these mutations effect myofilament sliding in human myocardium. Read More

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http://dx.doi.org/10.1016/j.yjmcc.2018.12.003DOI Listing
February 2019
1 Read