Mitochondrial dysfunction in acute kidney injury

Ren Fail. 2024 Dec;46(2):2393262. doi: 10.1080/0886022X.2024.2393262. Epub 2024 Aug 27.

Abstract

Acute kidney injury (AKI) is a systemic clinical syndrome increasing morbidity and mortality worldwide in recent years. Renal tubular epithelial cells (TECs) death caused by mitochondrial dysfunction is one of the pathogeneses. The imbalance of mitochondrial quality control is the main cause of mitochondrial dysfunction. Mitochondrial quality control plays a crucial role in AKI. Mitochondrial quality control mechanisms are involved in regulating mitochondrial integrity and function, including antioxidant defense, mitochondrial quality control, mitochondrial DNA (mtDNA) repair, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Currently, many studies have used mitochondrial dysfunction as a targeted therapeutic strategy for AKI. Therefore, this review aims to present the latest research advancements on mitochondrial dysfunction in AKI, providing a valuable reference and theoretical foundation for clinical prevention and treatment of this condition, ultimately enhancing patient prognosis.

Keywords: Acute kidney injury; mitochondrial biogenesis; mitochondrial dynamics; mitochondrial quality control; mitophagy.

Publication types

  • Review

MeSH terms

  • Acute Kidney Injury* / etiology
  • Acute Kidney Injury* / metabolism
  • Animals
  • Antioxidants / therapeutic use
  • DNA, Mitochondrial*
  • Epithelial Cells / metabolism
  • Humans
  • Kidney Tubules / pathology
  • Mitochondria* / metabolism
  • Mitochondrial Dynamics
  • Mitophagy*
  • Oxidative Stress

Substances

  • DNA, Mitochondrial
  • Antioxidants

Grants and funding

This research was funded by The National Natural Science Foundation of China [Grant Number: 82072222]; the Science and Technology Fund of Tianjin Municipal Education Commission [grant number: 2021KJ216].