Chemokines in healing myocardial infarction

NARRATIVE Members of the Transforming Growth Factor (TGF)- family are critically involved in regulation of inflammation and in repair following myocardial infarction; however, effective repair is dependent on timely inhibition of TGF- signaling to prevent persistent fibrogenic and hypertrophic responses The current proposal will investigate the mechanisms responsible for suppression and termination of TGF superfamily signaling cascades following infarction. In vivo experiments using cell-specific knockout mice and in vitro loss- and gain-of-function studies will be performed to dissect the molecular signals that inhibit TGF- responses in cardiomyocytes, fibroblasts and macrophages, thus protecting the infarcted heart from adverse remodeling.