Regulation of metabolism by miR-378 [PDF]
, 2014 The present invention provides a method of regulating fatty acid metabolism in a cell by contacting the cell with a modulator of miR-378 and/or miR-378* activity or expression.
Carrer, Michele, Olson, Eric N.
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Efficacy and Safety of Selective Cardiac Myosin Inhibitors in the Treatment of Hypertrophic Cardiomyopathy: a Meta-analysis [PDF]
Zhongguo quanke yixueBackground Hypertrophic cardiomyopathy (HCM) is a genetic disorder, characterized primarily by left ventricular outflow tract obstruction and asymmetric myocardial hypertrophy, which predisposes to sudden cardiac death and malignant arrhythmias. Although
ZHANG Huijuan, LI Xinghui, ZHANG Xiaoming, YIN Long, SHAO Long
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Aldosterone inhibits the fetal program and increases hypertrophy in the heart of hypertensive mice. [PDF]
PLoS ONE, 2012 BACKGROUND: Arterial hypertension (AH) induces cardiac hypertrophy and reactivation of "fetal" gene expression. In rodent heart, alpha-Myosin Heavy Chain (MyHC) and its micro-RNA miR-208a regulate the expression of beta-MyHC and of its intronic miR-208b.
Feriel Azibani +12 more
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Cardiac myosin inhibitor, mavacamten, improves myocardial relaxation in mouse HFpEF model
Cardiovascular Research, 2022 Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Medical Research Council (NMRC) Background / Introduction There are currently no treatments for ...
YH Lin +5 more
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Antibodies aggravate the development of ischemic heart failure [PDF]
, 2018 Heart-specific antibodies have been widely associated with myocardial infarction (MI). However, it remains unclear whether autoantibodies mediate disease progression or are a byproduct of cardiac injury. To disambiguate the role of immunoglobulins in MI,
Frantz, Stefan +6 more
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Pinocembrin Protects Cardiomyocytes Against Isoproterenol-Induced Hypertrophy
Natural Product Communications, 2021 Cardiac hypertrophy is characterized by an increase in myocardial cell volume and extracellular matrix production. Persistent cardiac hypertrophy can cause dilated cardiomyopathy, heart failure, and even death.
Xin Sui +7 more
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Onset of experimental severe cardiac fibrosis is mediated by overexpression of angiotensin-converting enzyme 2 [PDF]
, 2009 Angiotensin-converting enzyme (ACE) 2 is a recently identified homologue of ACE. There is great interest in the therapeutic benefit for ACE2 overexpression in the heart.
Allen, James M. +12 more
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Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 2022 Background Heart failure, caused by sustained pressure overload, remains a major public health problem. PKM (pyruvate kinase M) acts as a rate‐limiting enzyme of glycolysis. PKM2 (pyruvate kinase M2), an alternative splicing product of PKM, plays complex
Le Ni +7 more
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Heat Shock Protein 20 (HSP20) is a novel substrate for Protein Kinase D1 (PKD1) [PDF]
, 2015 Heat shock protein 20 (HSP20) has cardioprotective qualities, which are triggered by PKA phosphorylation. PKD1 is also a binding partner for HSP20, and this prompted us to investigate whether the chaperone was a substrate for PKD1.
Baillie, George, Sin, Yuan Yan
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Revisiting Frank–Starling: regulatory light chain phosphorylation alters the rate of force redevelopment (ktr) in a length-dependent fashion [PDF]
, 2016 Force and power in cardiac muscle have a known dependence on phosphorylation of the myosin-associated regulatory light chain (RLC). We explore the effect of RLC phosphorylation on the ability of cardiac preparations to redevelop force (ktr ) in maximally
Abraham +72 more
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