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Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
12:27

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ATF3 protects against renal ischemia-reperfusion injury

Takumi Yoshida1, Hidekazu Sugiura, Michihiro Mitobe

  • 1Department of Internal Medicine IV, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-city, Tokyo, Japan 162-8666. tyoshida@kc.twmu.ac.jp

Journal of the American Society of Nephrology : JASN
|February 1, 2008
PubMed

Insights

Activating transcription factor 3 (ATF3) protects against kidney injury caused by oxidative stress. Overexpressing ATF3 reduced cell death in kidney cells and decreased injury in a mouse model, offering a potential therapeutic target.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Oxidative stress contributes significantly to the progression of ischemic acute renal failure.
  • Identifying novel therapeutic targets is crucial for treating kidney injury.

Purpose of the Study:

  • To identify stress-induced genes as potential therapeutic candidates for ischemic acute renal failure.
  • To investigate the role of activating transcription factor 3 (ATF3) in oxidative stress-induced kidney injury.

Main Methods:

  • Microarray analysis of hydrogen peroxide (H2O2)-treated human proximal tubule (HK2) cells.
  • Adenovirus-mediated gene transfer to overexpress ATF3 in HK2 cells and a mouse model of renal ischemia-reperfusion injury.

Main Results:

  • Five genes, including ATF3, were significantly induced by H2O2 in HK2 cells.
  • ATF3 expression was upregulated by H2O2 and in a mouse model of renal ischemia-reperfusion injury.
  • Overexpression of ATF3 protected HK2 cells from H2O2-induced death and reduced injury in mice, associated with altered p53 and p21 mRNA levels.

Conclusions:

  • ATF3 plays a protective role in mitigating renal ischemia-reperfusion injury.
  • The protective mechanism of ATF3 may involve the suppression of p53 and induction of p21.
  • ATF3 represents a promising therapeutic candidate for acute kidney injury.

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