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.

Keywords:

• acute kidney injury
• Bid
• apoptosis
• Bcl-2 family protein
• ischemia