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Oxidized Albumin Induces Renal Tubular Cell Death and Promotes the Progression of Renal Diseases Through Ferroptosis

  • 0Division of Molecular Signaling, Department of the Advanced Biomedical Research, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Yamanashi 409-3898, Japan.
International Journal of Molecular Sciences +

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July 12, 2025

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July 12, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Oxidized albumin (ox-Alb) triggers kidney cell death via ferroptosis, a process involving specific protein and iron changes. This finding highlights ox-Alb

Area Of Science

  • Biochemistry
  • Cell Biology
  • Nephrology

Background

  • Oxidative stress is a key factor in disease.
  • Oxidized proteins, such as oxidized albumin (ox-Alb), may contribute to tissue damage.
  • The precise role of ox-Alb in kidney injury is not well understood.

Purpose Of The Study

  • To investigate the direct effects of ox-Alb on renal cells.
  • To elucidate the mechanisms by which ox-Alb causes kidney injury.
  • To determine if ox-Alb plays a role in ferroptosis.

Main Methods

  • Oxidation of albumin using copper/vitamin C.
  • In vitro studies using cultured renal tubular epithelial cells (NRK-52E).
  • In vivo mouse models of renal injury (vitamin C/copper, ischemia/reperfusion, doxorubicin-induced nephropathy).

Main Results

  • Ox-Alb induced cell death in renal tubular cells, linked to protein carbonylation and p38 MAPK activation.
  • Ox-Alb triggered ferroptosis in renal cells, characterized by altered GPX4, xCT, ACSL4, iron levels, and lipid peroxidation.
  • Administration of ox-Alb worsened doxorubicin-induced nephropathy in mice and intensified renal ferroptotic markers.

Conclusions

  • Oxidized albumin directly induces ferroptosis in renal cells.
  • Ox-Alb exacerbates kidney injury and promotes disease progression in oxidative stress-related kidney diseases.
  • Ox-Alb represents a significant pathogenic factor in kidney diseases associated with oxidative stress.

Keywords:

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