Mechanosensitive-mediated interaction, integration, and cardiac control.
This review covers aspects of the cardiac mechanotransduction field at different levels, and advocates the possibility that mechanoelectro-chemical transduction forms part of a network of mechanically linked integration in heart-mechanically mediated integration (MMI). It assembles evidence and observations in the literature to promote this hypothesis. Mechanical components can provide the bond between interactions at molecular, cellular, and macro levels to enable the integration. Stretch-activated channels (SACs) exist in the heart, but stresses and strains can affect other membrane channels or receptors. A cellular mechanical change can thus promote several ionic or downstream changes. Cell signal cascades have been implicated and can affect membrane electrophysiology. MMI could shape intracellular and downstream signals using the cytoskeleton and intracellular Ca(2+). MMI also spans other regulatory systems and processes such as the autonomic nervous system (ANS) and operates throughout the whole heart as an integrative system. Finally, supporting the hypothesis, if elements of the normal integration become deranged it contributes to cardiovascular disease and, potentially, lethal arrhythmia.
Lab
Max J
MJ
Imperial College, National Heart and Lung Institute, Charing Cross Campus, London W6 8RF, United Kingdom. m.lab@imperial.ac.uk
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002303:Cardiac Output, Low / Q000378:metabolism / Q000503:physiopathology; D006321:Heart / Q000502:physiology*; D006801:Humans; D040542:Mechanotransduction, Cellular
D002118:Calcium