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  • Mechano-regulation of the beating heart at the cellular level–Mechanosensitive channels in normal and diseased heart

    Author(s)
    Friedrich, Oliver
    Wagner, Soeren
    Battle, Andrew R
    Schuermann, Sebastian
    Martinac, Boris
    Griffith University Author(s)
    Battle, Andrew
    Year published
    2012
    Metadata
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    Abstract
    The heart as a contractile hollow organ finely tunes mechanical parameters such as stroke volume, stroke pressure and cardiac output according to filling volumes, filling pressures via intrinsic and neuronal routes. At the cellular level, cardiomyocytes in beating hearts are exposed to large mechanical stress during successive heart beats. Although the mechanisms of excitation–contraction coupling are well established in mammalian heart cells, the putative contribution of mechanosensitive channels to Ca2+ homeostasis, Ca2+ signaling and force generation has been primarily investigated in relation to heart disease states. For ...
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    The heart as a contractile hollow organ finely tunes mechanical parameters such as stroke volume, stroke pressure and cardiac output according to filling volumes, filling pressures via intrinsic and neuronal routes. At the cellular level, cardiomyocytes in beating hearts are exposed to large mechanical stress during successive heart beats. Although the mechanisms of excitation–contraction coupling are well established in mammalian heart cells, the putative contribution of mechanosensitive channels to Ca2+ homeostasis, Ca2+ signaling and force generation has been primarily investigated in relation to heart disease states. For instance, transient receptor potential channels (TRPs) are up-regulated in animal models of congestive heart failure or hypertension models and seem to play a vital role in pathological Ca2+ overload to cardiomyocytes, thus aggravating the pathology of disease at the cellular level. Apart from that, the contribution of mechanosensitive channels (MsC) in the normal beating heart to the downstream force activation cascade has not been addressed. We present an overview of the current literature and concepts of mechanosensitive channel involvement in failing hearts and cardiomyopathies and novel data showing a likely contribution of Ca2+ influx via mechanosensitive channels in beating normal cardiomyocytes during systolic shortening.
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    Journal Title
    Progress in Biophysics and Molecular Biology
    Volume
    110
    Issue
    2-3
    DOI
    https://doi.org/10.1016/j.pbiomolbio.2012.08.009
    Subject
    Biochemistry and cell biology
    Zoology not elsewhere classified
    Publication URI
    http://hdl.handle.net/10072/51750
    Collection
    • Journal articles

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