The platelet GARP/TGFb pathway in post-myocardial infarction healing

After myocardial infarction (MI), the damaged heart tissue triggers an inflammatory phase, which ultimately leads to fibrosis and adverse left ventricular remodelling. Transforming growth factor-β1 (TGF-β1) is recognized as a pivotal regulator of both inflammation and fibrosis. Platelets, which rapidly accumulate within the infarcted myocardium, are known to produce significant amounts of latent TGF-β1. Platelets can also produce active TGF-β1 via a mechanism that implies Glycoprotein A Repetitions Predominant (GARP) on their surface. In the present work, we investigate the role of platelet GARP protein in post-MI healing. Our results reveal that mice with a platelet-specific GARP deletion (pGARP KO) exhibit higher rates of myocardial rupture and exacerbated left ventricular dilatation following MI. This results from an enhanced inflammatory response, which impairs cardiac healing.