title: Regulation and pathological role of bid in ischemic acute kidney injury.
abstract: 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.
authors: Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
authors: Qingqing
authors: Q
authors: Wei
authors: Zheng
authors: Z
authors: Dong
mesh_terms: D058186:Acute Kidney Injury / Q000378:metabolism*; D000818:Animals; D051023:BH3 Interacting Domain Death Agonist Protein / Q000378:metabolism*
chemical_list: D051023:BH3 Interacting Domain Death Agonist Protein