Research ArticleCardiovascular Physiology

Convergence of G Protein–Coupled Receptor and S-Nitrosylation Signaling Determines the Outcome to Cardiac Ischemic Injury

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Sci. Signal.  29 Oct 2013:
Vol. 6, Issue 299, pp. ra95
DOI: 10.1126/scisignal.2004225

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NO More Heart Damage

Damage caused by the lack of oxygen and nutrients that occurs during myocardial ischemia can result in heart failure. A therapeutic strategy that helps to limit the effects of heart failure is to increase signaling through G protein–coupled receptors (GPCRs) by inhibiting GRK2 (GPCR kinase 2), a kinase that desensitizes GPCRs. Another therapeutic strategy provides S-nitrosothiols, such as nitric oxide, which can be added to proteins in a posttranslational modification called S-nitrosylation. Huang et al. found that the ability of S-nitrosothiols to enhance cardiomyocyte survival after ischemic injury required the S-nitrosylation of GRK2, a modification that inhibits this kinase. Mice bearing a form of GRK2 that could not be S-nitrosylated were more susceptible to cardiac damage after ischemia. These results suggest that therapeutic strategies that promote the S-nitrosylation of GRK2 could be used to treat heart failure after myocardial ischemia.