Research ArticleCardiovascular Physiology

RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis

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Science Signaling  21 Oct 2014:
Vol. 7, Issue 348, pp. ra100
DOI: 10.1126/scisignal.2005262

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Separating Cardiac Hypertrophy and Fibrosis

Over time, overloaded hearts typically become larger (a process called compensatory hypertrophy) to deal with the increased pressure. If prolonged, as occurs in untreated hypertension, the pressure overload leads to pathological hypertrophy and fibrosis, and ultimately leading to heart failure. Lauriol et al. found that mice with a cardiomyocyte-specific deficiency of RhoA, a GTP (guanosine 5′-triphosphate)–regulated protein, developed increased pathological hypertrophy but reduced fibrosis with chronic cardiac stress. These results suggest that targeting downstream effectors of RhoA, rather than RhoA itself, may be better for treating pathologies associated with heart failure.

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