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Transcription Factor ATF3 Mediating SOCS3 Expression Aggravates Renal Ischemia-Reperfusion Injury by Activating

Yu Luo1,2, Zhitao Cai2, Xiongfei Wu2

  • 1Department of Urology, Wuhan Sixth Hospital Affiliated Hospital of Jianghan University, Wuhan, China.

Nephron
|November 13, 2023
PubMed
Abstract

Insights

Suppressor of cytokine signaling 3 (SOCS3) exacerbates kidney injury by promoting mitophagy. Activating transcription factor 3 (ATF3) drives SOCS3 expression, worsening renal ischemia/reperfusion injury.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cellular Biology

Background:

  • Renal ischemia/reperfusion (RI/R) injury is a significant clinical challenge.
  • Suppressor of cytokine signaling 3 (SOCS3) is implicated in RI/R injury and mitophagy regulation.

Purpose of the Study:

  • To investigate the mechanism by which SOCS3 influences RI/R injury through mitophagy regulation.
  • To identify upstream regulators of SOCS3 in the context of RI/R injury.

Main Methods:

  • Established RI/R mouse and hypoxia/reoxygenation (H/R) cell models.
  • Assessed kidney damage and mitophagy using biochemical assays, molecular biology techniques, and histological analysis.
  • Identified and validated the interaction between ATF3, SOCS3, and IGF1R using database analysis and various binding assays.

Main Results:

  • RI/R injury models showed elevated BUN and creatinine, confirming successful induction.
  • SOCS3 expression was upregulated in RI/R mice; silencing SOCS3 alleviated kidney damage and inhibited mitophagy.
  • Activating transcription factor 3 (ATF3) was identified as a direct binder to the SOCS3 promoter, influencing its expression.

Conclusions:

  • ATF3 mediates SOCS3 expression, promoting mitophagy and exacerbating RI/R injury.
  • Targeting the ATF3-SOCS3 pathway may offer a therapeutic strategy for RI/R injury.
Keywords:
Activating transcription factor 3Acute kidney injuryInsulin-like growth factor 1 receptorMitophagySuppressor of cytokine signaling 3

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