Figure 7.

Schematic representation of Hsp90-mediated resistance to heat-stress damage in the kidney. Heat stress induced obvious renal histopathological and oxidative injury, which was connected with cellular apoptosis and autophagy. Under the assistance of Hsp70, Hsp90 played an important role in resisting apoptosis through the PKM2-Akt-HSF-1 axis and inducing autophagy-mediated survival through HIF-1α-BNIP3/BNIP3L signaling, ultimately protecting the kidney from heat stress-induced injury. In addition, the nuclear translocation of p-Akt and HSF-1 was instrumental in regulating the cellular ability of resisting heat-stress injury.