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- W630813294 abstract "Heart failure (HF) is a disease of epidemic proportion associated with exceedingly high healthcare costs. Data shows that G protein-coupled receptor (GPCR) kinase 2 (GRK2) plays a critical role in HF progression, promoting dysfunctional adrenergic signaling and myocyte death. We found that the selective serotonin reuptake inhibitor, paroxetine, could selectively inhibit GRK2. In this study wild-type mice underwent myocardial infarction (MI) and following 2 weeks of injury, underwent 4 weeks of treatment with paroxetine or control SSRI, fluoxetine. All post-MI mice exhibited similar left ventricular (LV) dysfunction prior to treatment; however, in contrast to continuing degradation of function, paroxetine produced significant improvement in LV function and structure. Paroxetine enhanced hemodynamic function, blocking the ~2.5 fold increase in LV end diastolic pressure (LVEDP). Paroxetine restored βAR membrane density, returned serum catecholamine and GRK2 levels to baseline, and prevented induction of the fetal gene program. Importantly, the beneficial effects persisted after termination of treatment and were markedly greater than β-blocker therapy, a current standard of care. These data demonstrate that paroxetine-mediated inhibition of GRK2 improves cardiac function post-MI and potentially represents novel re-purposing as well as a starting point for innovative small molecule inhibitor development." @default.
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- W630813294 date "2015-04-01" @default.
- W630813294 modified "2023-09-28" @default.
- W630813294 title "Paroxetine‐mediated GRK2 Inhibition Reverses Cardiac Dysfunction and Remodeling Post‐Myocardial Infarction" @default.
- W630813294 doi "https://doi.org/10.1096/fasebj.29.1_supplement.942.13" @default.
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