Regulation and pathological role of bid in ischemic acute kidney injury

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4 Scopus citations


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 languageEnglish (US)
Pages (from-to)935-940
Number of pages6
JournalRenal Failure
Issue number8
StatePublished - Nov 2007


  • Acute kidney injury
  • Apoptosis
  • Bcl-2 family protein
  • Bid
  • Ischemia

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Nephrology


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