chir-99021 and Atrial-Fibrillation

Healthy aging results in cardiac structural and electrical remodeling that increases susceptibility to cardiovascular diseases. Relaxin, an insulin-like hormone, suppresses atrial fibrillation, inflammation and fibrosis in aged rats but the mechanisms-of-action are unknown. Here we show that relaxin treatment of aged rats reverses pathological electrical remodeling (increasing Nav1.5 expression and localization of Connexin43 to intercalated disks) by activating canonical Wnt signaling. In isolated adult ventricular myocytes, relaxin upregulated Nav1.5 (EC

Topics: Adult; Age Factors; Aged; Animals; Atrial Fibrillation; Cells, Cultured; Fibroblasts; Fibrosis; Glycogen Synthase Kinase 3 beta; Healthy Aging; Humans; Isolated Heart Preparation; Male; Myocardium; Myocytes, Cardiac; Primary Cell Culture; Pyridines; Pyrimidines; Rats; Relaxin; Ventricular Remodeling; Wnt Signaling Pathway; Wnt1 Protein