TY  - GEN
A1  - Münch, Juliane
A1  - Abdelilah-Seyfried, Salim
T1  - Sensing and Responding of Cardiomyocytes to Changes of Tissue Stiffness in the Diseased Heart
T2  - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
N2  - Cardiomyocytes are permanently exposed to mechanical stimulation due to cardiac contractility. Passive myocardial stiffness is a crucial factor, which defines the physiological ventricular compliance and volume of diastolic filling with blood. Heart diseases often present with increased myocardial stiffness, for instance when fibrotic changes modify the composition of the cardiac extracellular matrix (ECM). Consequently, the ventricle loses its compliance, and the diastolic blood volume is reduced. Recent advances in the field of cardiac mechanobiology revealed that disease-related environmental stiffness changes cause severe alterations in cardiomyocyte cellular behavior and function. Here, we review the molecular mechanotransduction pathways that enable cardiomyocytes to sense stiffness changes and translate those into an altered gene expression. We will also summarize current knowledge about when myocardial stiffness increases in the diseased heart. Sophisticated in vitro studies revealed functional changes, when cardiomyocytes faced a stiffer matrix. Finally, we will highlight recent studies that described modulations of cardiac stiffness and thus myocardial performance in vivo. Mechanobiology research is just at the cusp of systematic investigations related to mechanical changes in the diseased heart but what is known already makes way for new therapeutic approaches in regenerative biology.
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1234 
KW  - mechanobiology
KW  - tissue stiffness
KW  - cardiomyocyte
KW  - heart regeneration
KW  - titin
KW  - collagen
KW  - agrin
KW  - extracellular matrix
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-545805
SN  - 1866-8372
ER  - 
TY  - JOUR
A1  - Münch, Juliane
A1  - Abdelilah-Seyfried, Salim
T1  - Sensing and responding of cardiomyocytes to changes of tissue stiffness in the diseased heart
JF  - Frontiers in cell developmental biology
N2  - Cardiomyocytes are permanently exposed to mechanical stimulation due to cardiac contractility. Passive myocardial stiffness is a crucial factor, which defines the physiological ventricular compliance and volume of diastolic filling with blood. Heart diseases often present with increased myocardial stiffness, for instance when fibrotic changes modify the composition of the cardiac extracellular matrix (ECM). Consequently, the ventricle loses its compliance, and the diastolic blood volume is reduced. Recent advances in the field of cardiac mechanobiology revealed that disease-related environmental stiffness changes cause severe alterations in cardiomyocyte cellular behavior and function. Here, we review the molecular mechanotransduction pathways that enable cardiomyocytes to sense stiffness changes and translate those into an altered gene expression. We will also summarize current knowledge about when myocardial stiffness increases in the diseased heart. Sophisticated in vitro studies revealed functional changes, when cardiomyocytes faced a stiffer matrix. Finally, we will highlight recent studies that described modulations of cardiac stiffness and thus myocardial performance in vivo. Mechanobiology research is just at the cusp of systematic investigations related to mechanical changes in the diseased heart but what is known already makes way for new therapeutic approaches in regenerative biology.
KW  - mechanobiology
KW  - tissue stiffness
KW  - cardiomyocyte
KW  - heart regeneration
KW  - titin
KW  - collagen
KW  - agrin
KW  - extracellular matrix
Y1  - 2020
U6  - https://doi.org/10.3389/fcell.2021.642840
SN  - 2296-634X
VL  - 9
PB  - Frontiers Media
CY  - Lausanne
ER  -