HSPD1 and myocardial ischemia: In C57BL/6J mice that underwent coronary artery ligation a rapid rise of phosphorylated IRAK‐1 (TLR4‐MyD88 signaling pathway) and HSP60 intracellular depletion were seen owing to increased secretion into the extracellular space, with HSP60 ability to activate extrinsic apoptotic pathways in cardiomyocytes, via caspase‐8, perpetuating deleterious effects in myocardial ischemia.123