The role of TRPC6-mediated autophagy in myocardial ischaemia/reperfusion injury

Abstract Cell and body damage are encouraged by myocardial ischaemia/reperfusion injury (MI/RI). The pathophysiology of cardiac I/R damage is mostly caused by oxidative stress, calcium excess, and inflammation. Cardiomyocytes' MI/RI is significantly influenced by autophagy. Through lysosome-mediated degradation, autophagy is a dynamic process that eliminates damaged organelles and long-lived proteins. This process has an antioxidant impact that lowers oxidative stress. An essential part of MI/RI is played by canonical transient receptor potential channel 6 (TRPC6), a nonselective cation channel that permits passage of Ca2+. It is yet unknown, nevertheless, how TRPC6 and autophagy relate to each other in MI/RI. In this work, we observed that following myocardial/ischaemia-reperfusion, autophagy and apoptosis increased, and that the production of autophagosomes and autophagy-related proteins, the Bax/Bcl-2 ratio, and cell damage decreased under TRPC6 suppression or knockout. Myocardial ischaemia/reperfusion injury may benefit from targeting TRPC6-mediated autophagy as a potential novel therapeutic target in the future.