Regulation and pathological role of bid in ischemic acute kidney injury

Research output: Contribution to journalReview article

4 Citations (Scopus)

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 languageEnglish (US)
Pages (from-to)935-940
Number of pages6
JournalRenal Failure
Volume29
Issue number8
DOIs
StatePublished - Nov 1 2007

Fingerprint

Acute Kidney Injury
Kidney
Reperfusion
Ischemia
Wounds and Injuries
Adenosine Triphosphate
Research
Proteins

Keywords

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

ASJC Scopus subject areas

  • Nephrology

Cite this

Regulation and pathological role of bid in ischemic acute kidney injury. / Wei, QingQing; Dong, Zheng.

In: Renal Failure, Vol. 29, No. 8, 01.11.2007, p. 935-940.

Research output: Contribution to journalReview article

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