FAK regulates cardiomyocyte mitochondrial fission and function through Drp1

• DOI: 10.1111/febs.16263
• Publication Date: 2021-11-05T16:40:35Z
• Authors: Yu‐Wang Chang; Zong‐Han Song; Chien‐Chang Chen
• Keywords: Dynamins; 0301 basic medicine; 03 medical and health sciences; Focal Adhesion Protein-Tyrosine Kinases; Animals; Myocytes, Cardiac; Phosphorylation; Mitochondrial Dynamics; Rats

Loss of the mitochondrial fission enzyme dynamin-related protein 1 (Drp1) in cardiomyocytes results energy shortage and heart failure. We aim to understand intracellular signal pathway extracellular factors regulating Drp1 phosphorylation morphology function cardiomyocytes. found cyclic mechanical stretching induced through focal adhesion kinase (FAK) neonatal rat ventricular myocytes (NRVMs). FAK regulated levels. Extracellular fibronectin activated caused signal-regulated 1/2 (ERK1/2). Fibronectin increased NRVMs oxygen consumption rate ATP content via FAK-ERK1/2-Drp1. Inhibition FAK-ERK1/2-Drp1 cellular shortage. In addition, was rapidly by adrenergic agonists contributed agonists-stimulated respiration. Interestingly, limited agonists-induced respiration restricting Drp1. Our suggest that stimulations use regulate