Results 31 to 40 of about 51,825 (261)

Aldosterone inhibits the fetal program and increases hypertrophy in the heart of hypertensive mice. [PDF]

open access: yesPLoS 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
doaj   +1 more source

Pyruvate Kinase M2 Protects Heart from Pressure Overload‐Induced Heart Failure by Phosphorylating RAC1

open access: yesJournal 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
doaj   +1 more source

Heat Shock Protein 20 (HSP20) is a novel substrate for Protein Kinase D1 (PKD1) [PDF]

open access: yes, 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
core   +1 more source

Cardiac myosin inhibitor, mavacamten, improves myocardial relaxation in mouse HFpEF model

open access: yesCardiovascular 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
openaire   +1 more source

Cell-based gene therapy for mending infarcted hearts [PDF]

open access: yes, 2011
The goal of this study was to analyse the efficiency of a combinatorial cell/growth factor therapy to improve function of infarcted murine hearts. The Insulin-like Growth Factor-1 (IGF-1) isoform, IGF-1Ea, has been shown to reduce scar formation and ...
Poudel, Bhawana, Poudel, Bhawana
core   +1 more source

HIF1α-dependent mitophagy facilitates cardiomyoblast differentiation [PDF]

open access: yes, 2020
Mitophagy is thought to play a key role in eliminating damaged mitochondria, with diseases such as cancer and neurodegeneration exhibiting defects in this process.
Allen, George F. G.   +4 more
core   +3 more sources

Micro-RNAS that control myosin expression and myofiber identity [PDF]

open access: yes, 2015
The present invention relates to the identification of two microRNAs, miR-499 and miR-208b, that repress fast skeletal muscle contractile protein genes. Expression of miR-499 and/or miR-208b can be used to repress fast fiber genes and activate slow fiber
Olson, Eric N., van Rooij, Eva
core   +1 more source

Rescue of Pressure Overload-Induced Heart Failure by Estrogen Therapy. [PDF]

open access: yes, 2016
BackgroundEstrogen pretreatment has been shown to attenuate the development of heart hypertrophy, but it is not known whether estrogen could also rescue heart failure (HF).
Bopassa, Jean C   +12 more
core   +1 more source

Cardiomyocyte Specific Deletion of ADAR1 Causes Severe Cardiac Dysfunction and Increased Lethality

open access: yesFrontiers in Cardiovascular Medicine, 2020
Background: Adenosine deaminase acting on RNA 1 (ADAR1) is a double-stranded RNA-editing enzyme that is involved in several functions including the deamination of adenosine to inosine, RNA interference (RNAi) mechanisms and microRNA (miRNA) processing ...
Hamid el Azzouzi   +11 more
doaj   +1 more source

Progress in New Therapies Targeting the Pathogenesis of Cardiomyopathywith Hypertrophic Phenotype

open access: yes罕见病研究, 2023
Hypertrophic cardiomyopathy (HCM) is cardiomyopathy with a clinical phenotype of cardiac hypertrophy. The etiology includes genetically defective encoding sarcomeres, congenital metabolic diseases such as lysosomal storage diseases, systemic amyloidosis ...
LIU Yanbo, TIAN Zhuang, ZHANG Shuyang
doaj   +1 more source

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