Research ArticleHeart Failure

Paroxetine-mediated GRK2 inhibition reverses cardiac dysfunction and remodeling after myocardial infarction

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Science Translational Medicine  04 Mar 2015:
Vol. 7, Issue 277, pp. 277ra31
DOI: 10.1126/scitranslmed.aaa0154

Taking antidepressants to heart

Drug repurposing—extending currently Food and Drug Administration (FDA)–approved drugs to treat additional diseases—has both economic and safety advantages over new drug development. The selective serotonin reuptake inhibitor (SSRI) paroxetine, which is used as an antidepressant, has been shown to selectively inhibit G protein (heterotrimeric guanine nucleotide–binding protein)–coupled receptor kinase 2 (GRK2), which is thought to contribute to heart failure progression. Now Schumacher et al. report that paroxetine can block or even reverse heart damage after myocardial infarction in a mouse model. These affects are separate from its SSRI functions and are further enhanced in the presence of current standard-of-care β-blockers. If these data hold true in humans, paroxetine therapy could be an additional or even additive strategy for treating heart failure.

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