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Related Experiment Video

Updated: Jul 3, 2026

Assay Development for High Content Quantification of Sod1 Mutant Protein Aggregate Formation in Living Cells
11:12

Assay Development for High Content Quantification of Sod1 Mutant Protein Aggregate Formation in Living Cells

Published on: October 4, 2017

Pathological Copper Overload Reprograms SOD1 Activation via COMMD1 to Promote Senescence and Fibrosis.

Yuqing Liu1, Jing Liu1, Wenqian Zhou1

  • 1Department of Nephrology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|July 2, 2026
PubMed
Summary

Pathological copper overload paradoxically inhibits the antioxidant enzyme superoxide dismutase 1 (SOD1) by disrupting its homodimerization via COMMD1. Restoring copper balance reactivates SOD1, reducing kidney fibrosis and senescence.

Keywords:
cellular senescencecopper homeostasiscopper metabolism MURR1 domain containing 1 (COMMD1)renal fibrosissuperoxide dismutase 1 (SOD1)

Related Experiment Videos

Last Updated: Jul 3, 2026

Assay Development for High Content Quantification of Sod1 Mutant Protein Aggregate Formation in Living Cells
11:12

Assay Development for High Content Quantification of Sod1 Mutant Protein Aggregate Formation in Living Cells

Published on: October 4, 2017

Area of Science:

  • Biochemistry
  • Cell Biology
  • Renal Pathophysiology

Background:

  • Superoxide dismutase 1 (SOD1) is a critical antioxidant enzyme for maintaining redox balance.
  • Reduced SOD1 activity is linked to kidney senescence and fibrosis in chronic kidney disease (CKD).
  • Mechanisms connecting profibrotic signaling to SOD1 inhibition are not fully understood.

Purpose of the Study:

  • To investigate the role of copper in regulating SOD1 activity in kidney fibrosis.
  • To elucidate the molecular mechanisms by which copper overload suppresses SOD1 function.
  • To identify potential therapeutic targets for copper dyshomeostasis-related kidney diseases.

Main Methods:

  • Analysis of kidney tissues from CKD patients.
  • In vivo and in vitro studies using fibrotic models.
  • Assessment of SOD1 activity, intracellular copper levels, and reactive oxygen species (ROS).
  • Investigation of SOD1 homodimerization and COMMD1-SOD1 interactions.

Main Results:

  • CKD patients and fibrotic models showed reduced SOD1 activity and elevated intracellular copper.
  • Lowering intracellular copper restored SOD1 activity, decreased ROS, and alleviated senescence and fibrosis.
  • Pathological copper overload upregulated COMMD1 expression and enhanced its binding to SOD1.
  • This interaction disrupted SOD1 homodimerization and enzymatic function.

Conclusions:

  • A pathological copper-COMMD1-SOD1 axis suppresses SOD1 activity in kidney fibrosis.
  • Copper overload impairs SOD1 function by disrupting its homodimerization via COMMD1.
  • Targeting copper metabolism offers a novel therapeutic strategy for kidney diseases associated with copper dyshomeostasis.