In a failing human heart there is an increase in the presence of G-protein-coupled receptor kinase 2 (GRK2). This enzyme hastens the onset of heart failure.
Researchers have observed that GRK2 could be inhibited by the selective serotonin reuptake inhibitor (SSRI) paroxetine. Therefore, mice with heart failure were used to compare paroxetine with fluoxetine, an SSRI that does not inhibit GRK2.
After two weeks, the mice given paroxetine had improved left ventricular function and structure and a regression of many signs of heart failure, in a study published in Science Translational Medicine
(online, 4 March 2015). Mice in the fluoxetine group had continued deterioration, indicating that the effect is independent of the serotonin system. In addition, paroxetine was more effective than beta blockers, which the authors note is currently the gold-standard human treatment.
 Schumacher S, Gao E, Zhu W et al. Paroxetine-mediated GRK2 inhibition reverses cardiac dysfunction and remodelling after myocardial infarction. Science Translational Medicine 2015;7:277ra31. doi: 10.1126/scitranslmed.aaa0154.