Blocking RIPK2 Function Alleviates Myocardial Ischemia/Reperfusion Injury by Regulating the AKT and NF-κB Pathways

Objective Inflammation and oxidation brought on by myocardial ischemia-reperfusion (MI/R) injury lead to cardiomyocyte apoptosis and necrosis. The receptor interacting serine/threonine kinase 2 (RIPK2) plays significant roles in oxidative stress and excessive inflammation. The purpose of this research is to examine the roles of RIPK2 in MI/R injury.