Cells in the myocardium are exposed to stretching forces from hemodynamic pressure or the cardiomyocyte contraction as well as passive elasticity from the extracellular matrix (ECM), all of which are subject to change during development and disease.
Especially cardiac diseases, such as hypertrophic cardiomyopathies are frequently associated with myocardial fibrosis, which stiffens the mechanical environment of the cardiomyocytes.
While several studies have investigated the role of matrix stiffness on contractile properties of cardiomyocytes it is still unclear how this is influencing disease progression by altering mechanosignalling pathways in cardiomyopathies or after cardiac infarction.
Moreover the molecular mechanism behind cardiomyocyte rigidity sensing are still elusive. Here we aim to address these critical questions, using neonatal rat and hIPS cardiomyocytes, together with tools to apply or measure forces as well as live- (superresolution) microscopy.