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.
Original language | English (US) |
---|---|
Pages (from-to) | 935-940 |
Number of pages | 6 |
Journal | Renal Failure |
Volume | 29 |
Issue number | 8 |
DOIs | |
State | Published - Nov 2007 |
Keywords
- Acute kidney injury
- Apoptosis
- Bcl-2 family protein
- Bid
- Ischemia
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
- Nephrology