Vinculin network–mediated cytoskeletal remodeling regulates contractile function in the aging heart

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Science Translational Medicine  17 Jun 2015:
Vol. 7, Issue 292, pp. 292ra99
DOI: 10.1126/scitranslmed.aaa5843

Sending in vinculin reinforcements

A common charge for graceful aging is to stay “young at heart.” With age, the heart undergoes necessary remodeling to keep it functioning—or young—even though the heart experiences relatively little regeneration in the human lifetime. The mechanisms of remodeling in mammals remain unclear but, if known, could help develop new therapies to treat heart failure, a leading killer in the developed world. Kaushik et al. therefore performed a proteomic analysis in old and young monkeys and rats, and identified one protein at the heart of it all: vinculin. Vinculin is conserved across species, being present at cell-matrix and cell-cell adhesions and also anchoring the cardiomyocyte membrane to its actin cytoskeleton. Thus, Kaushik et al. hypothesized that vinculin accumulates with age to regulate cytoskeletal stiffening and heart cell contractility. This mechanism was confirmed in rats and in different strains of Drosophila, supporting the notion that particular aspects of heart remodeling are beneficial and prolong life span, rather than being maladaptive. By using several models and producing a large proteomic network centered on vinculin and other cytoskeletal proteins, the authors have put forth a valuable resource for better understanding cardiac aging and for selecting therapeutic targets to prevent heart failure and also keep the heart young and beating as we age.

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