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Mitochondrial redox imbalance in triggering regulated cell death in kidney diseases

Wenping Zhu1,2,3, Ran Zou2,3, Ruotian Liu2,3

  • 1Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing 210008, China.

Iscience
|July 2, 2026
PubMed

Insights

Mitochondrial reactive oxygen species (mtROS) signal cell life but excessive mtROS causes kidney damage. Understanding mtROS-driven cell death pathways offers new therapeutic targets for kidney disease.

Area of Science:

  • Nephrology
  • Cell Biology
  • Biochemistry

Background:

  • Mitochondrial reactive oxygen species (mtROS) are vital for renal cell functions like immunity and autophagy.
  • An imbalance in mtROS production and antioxidant capacity leads to mtROS accumulation, causing cellular damage and oxidative stress.
  • Oxidative stress in the kidneys can trigger various forms of regulated cell death (RCD).

Purpose of the Study:

  • To review the role of mitochondrial redox imbalance in initiating RCD in kidney diseases.
  • To enhance understanding of cell death mechanisms in the context of kidney disorders.
  • To provide insights for developing mtROS-targeted therapeutics for kidney diseases.

Main Methods:

  • Literature review focusing on mitochondrial redox biology and kidney cell death.
  • Analysis of distinct genetic and biochemical features of various RCD types.
  • Synthesis of information on mtROS accumulation and its downstream effects.

Main Results:

  • Mitochondrial redox imbalance is a key initiator of diverse RCD pathways in the kidney.
  • Excessive mtROS disrupts cellular homeostasis by oxidizing critical macromolecules.
  • Specific RCD types discussed include autophagy, apoptosis, pyroptosis, ferroptosis, necroptosis, cuproptosis, and PANoptosis.

Conclusions:

  • Understanding mtROS-driven oxidative cell death is crucial for advancing kidney disease treatment.
  • Targeting mtROS pathways presents a promising therapeutic strategy for renal disorders.
  • Further research into specific RCD mechanisms can lead to novel therapeutic interventions.
Keywords:
Human metabolismNephrology

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