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  11. Mitochondrial Dysfunction-evoked Dhodh Acetylation Is Involved In Renal Cell Ferroptosis During Cisplatin-induced Acute Kidney Injury.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Mitochondrial Dysfunction-evoked Dhodh Acetylation Is Involved In Renal Cell Ferroptosis During Cisplatin-induced Acute Kidney Injury.

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Mitochondrial Dysfunction-Evoked DHODH Acetylation is Involved in Renal Cell Ferroptosis during Cisplatin-Induced Acute Kidney Injury.

Nan-Nan Liang1, Yue-Yue Guo1, Xiao-Yi Zhang1

  • 1Department of Toxicology, Anhui Medical University, Hefei, China, 230032.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|September 20, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Mitochondrial dysfunction drives DHODH acetylation, contributing to ferroptosis in cisplatin-induced acute kidney injury (AKI). Restoring SIRT3 or using antioxidants like MitoQ can protect against AKI and ferroptosis.

Keywords:
DHODH acetylationSIRT3 SUMOylationacute kidney injurycisplatin

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Area of Science:

  • Nephrology
  • Biochemistry
  • Cell Biology

Background:

  • Cisplatin-induced acute kidney injury (AKI) is associated with renal cell ferroptosis.
  • The precise mechanisms underlying cisplatin-induced ferroptosis remain unclear.

Purpose of the Study:

  • To elucidate the role of mitochondrial dysfunction and DHODH acetylation in cisplatin-induced AKI.
  • To investigate the involvement of SIRT3 in regulating DHODH acetylation and ferroptosis.

Main Methods:

  • Utilized cisplatin-treated HK-2 cells and mouse models of AKI.
  • Performed targeted metabolomics to analyze pyrimidine biosynthesis.
  • Assessed DHODH activity, acetylation, and CoQH2 levels.
  • Investigated the role of SIRT3 through overexpression, knockout, and NMN supplementation.
ferroptosis
  • Evaluated the effects of the mitochondria-targeted antioxidant MitoQ.

    • Main Results:

    • Cisplatin treatment increased oxidized arachidonic acid metabolites and decreased pyrimidine biosynthesis.
    • Mitochondrial DHODH and CoQH2 were downregulated, while DHODH acetylation and SIRT3 SUMOylation increased.
    • DHODH overexpression attenuated ferroptosis, whereas DHODH silence exacerbated it.
    • SIRT3 deficiency aggravated DHODH acetylation and ferroptosis, while SIRT3 overexpression and NMN supplementation offered protection.
    • MitoQ mitigated mitochondrial dysfunction, SIRT3 SUMOylation, DHODH acetylation, and ferroptosis.

    Conclusions:

    • Mitochondrial dysfunction-induced DHODH acetylation is a key mechanism in renal cell ferroptosis during cisplatin-induced AKI.
    • SIRT3 plays a protective role by deacetylating DHODH.
    • Targeting mitochondrial dysfunction and DHODH acetylation may offer therapeutic strategies for AKI.