Regulation and pathological role of bid in ischemic acute kidney injury.
Bid, a BH3-only member of the Bcl-2 family proteins, is most abundantly expressed in the kidneys. Recent research has shown Bid activation in renal tubular cells in vitro following ATP-depletion and hypoxic injury, and also in vivo during renal ischemia-reperfusion in rats and mice. Importantly, Bid-deficient mice are resistant to ischemic kidney injury. Targeting Bid may therefore offer a new strategy for the treatment of acute renal failure associated with ischemia-reperfusion.
Wei
Qingqing
Q
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
Dong
Zheng
Z
D058186:Acute Kidney Injury / Q000378:metabolism*; D000818:Animals; D051023:BH3 Interacting Domain Death Agonist Protein / Q000378:metabolism*
D051023:BH3 Interacting Domain Death Agonist Protein