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Review
. 2014 Jun;466(6):1093-9.
doi: 10.1007/s00424-014-1468-4. Epub 2014 Feb 16.

Mechano-signaling in heart failure

Byambajav Buyandelger  1 , Catherine Mansfield, Ralph Knöll
Affiliations
Review

Mechano-signaling in heart failure

Byambajav Buyandelger et al. Pflugers Arch. 2014 Jun.

Erratum in

  • Pflugers Arch. 2014 Sep;466(9):1845

Abstract

Mechanosensation and mechanotransduction are fundamental aspects of biology, but the link between physical stimuli and biological responses remains not well understood. The perception of mechanical stimuli, their conversion into biochemical signals, and the transmission of these signals are particularly important for dynamic organs such as the heart. Various concepts have been introduced to explain mechanosensation at the molecular level, including effects on signalosomes, tensegrity, or direct activation (or inactivation) of enzymes. Striated muscles, including cardiac myocytes, differ from other cells in that they contain sarcomeres which are essential for the generation of forces and which play additional roles in mechanosensation. The majority of cardiomyopathy causing candidate genes encode structural proteins among which titin probably is the most important one. Due to its elastic elements, titin is a length sensor and also plays a role as a tension sensor (i.e., stress sensation). The recent discovery of titin mutations being a major cause of dilated cardiomyopathy (DCM) also underpins the importance of mechanosensation and mechanotransduction in the pathogenesis of heart failure. Here, we focus on sarcomere-related mechanisms, discuss recent findings, and provide a link to cardiomyopathy and associated heart failure.

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Figures

Fig. 1
Fig. 1
Schematic representation of sarcomere-associated mechanosensory processes
See this image and copyright information in PMC

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