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SENP1 protects cisplatin-induced AKI by attenuating apoptosis through regulation of HIF-1α

Ling Wang1, Xiang Gao2, Xiaojing Tang2

  • 1Department of Nephrology & Rheumatology, Shanghai Tenth People's Hospital of Tongji University, No. 301 YanChang Road, Shanghai, 200072, China.

Experimental Cell Research
|July 15, 2022
PubMed
Abstract

Insights

SENP1 promotes kidney injury in acute kidney injury (AKI) by increasing cell apoptosis, while HIF-1α offers protection. Targeting the SENP1/HIF-1α axis may offer new treatments for AKI.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Acute kidney injury (AKI) presents significant morbidity and mortality, with unclear molecular mechanisms.
  • The role of SENP1 in AKI is unknown, despite its substrate HIF-1α having a known nephroprotective effect.

Purpose of the Study:

  • To elucidate the role of the SENP1/HIF-1α axis in the pathogenesis of AKI.
  • To investigate SENP1's function in AKI using cellular and animal models.

Main Methods:

  • Investigated SENP1 expression in clinical AKI samples and cisplatin-induced AKI models (mice and HK-2 cells).
  • Assessed the impact of SENP1 knockdown/overexpression on AKI.
  • Examined HIF-1α expression changes and the combined effects of SENP1 knockdown and HIF-1α overexpression.

Main Results:

  • SENP1 was upregulated in clinical specimens and AKI models.
  • SENP1 manipulation affected HK-2 cell apoptosis and AKI severity in mice.
  • HIF-1α overexpression counteracted the detrimental effects of SENP1 knockdown on apoptosis and AKI.

Conclusions:

  • SENP1 exacerbates kidney injury in AKI by regulating cell apoptosis and influencing HIF-1α.
  • The SENP1/HIF-1α pathway is a potential therapeutic target for AKI treatment.
Keywords:
Acute kidney injuryApoptosisCisplatinHIF-1αSENP1

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