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Mechanosensitive‐Mediated Interaction, Integration, and Cardiac Control
Author(s) -
LAB MAX J
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1380.022
Subject(s) - mechanosensitive channels , mechanotransduction , intracellular , neuroscience , microbiology and biotechnology , cytoskeleton , signal transduction , ion channel , biology , electrophysiology , receptor , chemistry , biophysics , cell , genetics
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.