Results 71 to 80 of about 180,856 (396)

A modeling framework for contact, adhesion and mechano-transduction between excitable deformable cells

open access: yes, 2017
Cardiac myocytes are the fundamental cells composing the heart muscle. The propagation of electric signals and chemical quantities through them is responsible for their nonlinear contraction and dilatation. In this study, a theoretical model and a finite
Gizzi, Alessio   +2 more
core   +1 more source

Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophy [PDF]

open access: yes, 2014
Chronic neurohormonal and mechanical stresses are central fea-tures of heart disease. Increasing evidence supports a role forthe transient receptor potential canonical channels TRPC3 andTRPC6 in this pathophysiology.
Andersen, Asger   +13 more
core   +1 more source

Hydrogen Peroxide–Mediated SERCA Cysteine 674 Oxidation Contributes to Impaired Cardiac Myocyte Relaxation in Senescent Mouse Heart

open access: yesJournal of the American Heart Association : Cardiovascular and Cerebrovascular Disease, 2013
Background A hallmark of aging of the cardiac myocyte is impaired sarcoplasmic reticulum (SR) calcium uptake and relaxation due to decreased SR calcium ATPase (SERCA) activity. We tested the hypothesis that H2O2‐mediated oxidation of SERCA contributes to
F. Qin   +10 more
semanticscholar   +1 more source

Cardiac Myocytes and Mechanosensation [PDF]

open access: yes, 2012
Mechanosensation is a fundamental process in biology and may have been developed by the early cells in response to hypo-osmotic stress [1]. With the evolution of different cell types and the appearance of multi-cellular organisms the mechanisms of mechanosensation and the corresponding transmission of signals became more complex and evolved in ...
Byambajav Buyandelger, Ralph Knöll
openaire   +3 more sources

Dystrophic cardiomyopathy: role of the cardiac myofilaments

open access: yesFrontiers in Physiology, 2023
Dystrophic cardiomyopathy arises from mutations in the dystrophin gene. Dystrophin forms part of the dystrophin glycoprotein complex and is postulated to act as a membrane stabilizer, protecting the sarcolemma from contraction-induced damage.
Thomas G. George   +4 more
doaj   +1 more source

The impact of Hnrnpl deficiency on transcriptional patterns of developing muscle cells

open access: yesFEBS Open Bio, EarlyView.
We performed nanopore whole‐transcriptome sequencing comparing RNA from Hnrnpl‐knockdown versus control C2C12 myoblasts to investigate the contributions of Hnrnpl to muscle development. Our results indicate that Hnrnpl regulates the expression of genes involved with Notch signaling and skeletal muscle, particularly splicing patterns of specific muscle ...
Hannah R. Littel   +8 more
wiley   +1 more source

Progressive Reduction in Myocyte Autophagy After Myocardial Infarction in Rabbits: Association with Oxidative Stress and Left Ventricular Remodeling

open access: yesCellular Physiology and Biochemistry, 2017
Background/Aims: The alterations in myocyte autophagy after myocardial infarction (MI) and the underlying mechanisms have not been fully understood. In this study, we investigated the temporal changes of myocyte autophagy in the remote non-infarcted ...
Rui-Fang Chi   +9 more
doaj   +1 more source

Redox signaling in cardiac myocytes

open access: yesFree Radical Biology and Medicine, 2011
The heart has complex mechanisms that facilitate the maintenance of an oxygen supply-demand balance necessary for its contractile function in response to physiological fluctuations in workload as well as in response to chronic stresses such as hypoxia, ischemia, and overload.
Xavier Da Costa Dos Santos, Celio Santos   +4 more
openaire   +4 more sources

Cardiac Myocyte Exosome Isolation [PDF]

open access: yes, 2016
Exosomes are cell-derived small extracellular membrane vesicles (50-100 nm in diameter) actively secreted by a number of healthy and diseased cell types. Exosomes can mediate cellular, tissue, and organ level micro communication under normal and pathological conditions by shuttling proteins, mRNA, and microRNAs.
Malik, Zulfiqar A   +2 more
openaire   +5 more sources

Growth Differentiation Factor 15 Elevation in the Central Nervous System Is Associated With Failure to Thrive in Alexander Disease

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Objective Alexander disease (AxD) is a severe neurodegenerative disorder caused by gain‐of‐function mutations in the gene for GFAP, which lead to protein aggregation and a primary astrocytopathy. Symptoms vary, but failure to thrive (FTT) and frequent emesis are common and cause significant morbidity. Here we investigate GDF15, a member of the
Tracy L. Hagemann   +6 more
wiley   +1 more source

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