European Journal of Cardiovascular Medicine

Almost any definition of biological life includes the term “movement”, which is inherently linked to the sensation of mechanically induced deformation. As such, mechanosensation (a cell’s perception of mechanical stimuli) as well as mechanotransduction (transmission of mechanically induced signals) belong to the most fundamental processes in biology. These processes are particularly important in cardiovascular physiology, as each cycle of contraction and relaxation causes dynamic deformations of the heart and the large blood vessels. Cardiomyocytes are equipped with different mechanisms aimed to sense any form of mechanical deviation. For example, the titin springs extend and unfold elastic domains during diastolic distension and may serve as a length sensor, in contrast to the Z-discs, which experience particularly high forces during systole and may serve as a tension sensor. Activation of different sensors at the cellular level affects the composition of signalosomes attached to these structures, and these signalling complexes eventually translate the mechanical information into functional alterations via short term (i.e., activation of kinases) or long term (i.e., altered gene expression) effects. At the organ level, mechanosensation is involved in diverse feedback mechanisms such as the Bainbridge reflex, the Frank-Starling mechanism, and ischemic preconditioning. Therefore, it is not surprising that mutations in components of the cardiomyocyte stretch sensory apparatus cause cardiomyopathy and heart failure. Although significant progress has been made in this field during the last decade, the molecular mechanisms underlying mechanosensation still remain poorly understood. The article offers an overview on the fundamental processes involved in cardiomyocyte stretch sensing and provides important links to clinical cardiology.