Figure 10.

Schematic diagram summarizing the protective effects of Hsp90 against heat stress injury of myocardial tissues via the activation of Akt and PKM2 signaling. The in vivo experiments showed that Hsp90 promotes Akt phosphorylation, its mitochondrial translocation, and PKM2 mitochondrial translocation, thereby increasing the downstream the levels of mitochondrial Bcl-2 and its phosphorylation. This contributes toward the preservation of cardiac function and mitochondrial homeostasis, and the alleviation of oxidative stress and apoptosis in heat-stressed cardiomyocytes. Furthermore, several pathways that include Hsp90 can activate Akt signaling and then regulate the levels Hsp70 through HSF-1. Hsp70 interacts with Hsp90 to influence its downstream proteins. Myocardial Hsp70 can leak out into the bloodstream to initiate another protective mechanism.