A potential role for integrin signaling in mechanoelectrical feedback

Borna E. Dabiri, Hyungsuk Lee, Kevin Kit Parker

Research output: Contribution to journalReview articlepeer-review

38 Citations (Scopus)


Certain forms of heart disease involve gross morphological changes to the myocardium that alter its hemodynamic loading conditions. These changes can ultimately lead to the increased deposition of extracellular matrix (ECM) proteins, such as collagen and fibronectin, which together work to pathologically alter the myocardium's bulk tissue mechanics. In addition to changing the mechanical properties of the heart, this maladaptive remodeling gives rise to changes in myocardium electrical conductivity and synchrony since the tissue's mechanical properties are intimately tied to its electrical characteristics. This phenomenon, called mechanoelectrical coupling (MEC), can render individuals affected by heart disease arrhythmogenic and susceptible to Sudden Cardiac Death (SCD). The underlying mechanisms of MEC have been attributed to various processes, including the action of stretch activated channels and changes in troponin C-Ca2+ binding affinity. However, changes in the heart post infarction or due to congenital myopathies are also accompanied by shifts in the expression of various molecular components of cardiomyocytes, including the mechanosensitive family of integrin proteins. As transmembrane proteins, integrins mechanically couple the ECM with the intracellular cytoskeleton and have been implicated in mediating ion homeostasis in various cell types, including neurons and smooth muscle. Given evidence of altered integrin expression in the setting of heart disease coupled with the associated increased risk for arrhythmia, we argue in this review that integrin signaling contributes to MEC. In light of the significant mortality associated with arrhythmia and SCD, close examination of all culpable mechanisms, including integrin-mediated MEC, is necessary.

Original languageEnglish
Pages (from-to)196-203
Number of pages8
JournalProgress in Biophysics and Molecular Biology
Issue number2-3
Publication statusPublished - 2012 Oct

Bibliographical note

Funding Information:
We would like to acknowledge comments by Ashutosh Agarwal, Francesco S. Pasqualini, and Sean Sheehy of the Disease Biophysics Group on the manuscript. This work was supported by NIH R01 HL079126 .

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Molecular Biology


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