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Updated: Aug 15, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease
Hsin-Jung Ho1, Hitoshi Shirakawa2,3
1Faculty of Health Sciences, Hokkaido University, Sapporo 060-0812, Japan.
Mitochondria play a crucial role in kidney function and energy production. This review explores how targeting mitochondria can prevent oxidative stress and protect against kidney disease, offering insights into new therapeutic strategies.
Area of Science:
- Nephrology
- Mitochondrial Biology
- Oxidative Stress Research
Background:
- Mitochondria are vital for kidney cellular energy (ATP) production.
- Impaired mitochondria and excessive reactive oxygen species cause oxidative stress injury.
- Oxidative stress is increasingly linked to kidney diseases, including chronic kidney disease.
Purpose of the Study:
- To review the relationship between mitochondria-targeted effects and kidney disease risk factors.
- To explore mitochondria-targeted therapeutics for renal injury.
- To summarize recent studies on oxidative stress and mitochondrial function in kidney diseases.
Main Methods:
- Integration of recent studies on oxidative stress and mitochondrial function in kidney diseases.
- Organization of causes and risk factors of kidney oxidative stress based on mitochondria-targeted effects.
- Identification of potential clinical therapeutics modulating mitochondrial function.
Main Results:
- Oxidative stress is a significant factor in kidney damage, often stemming from mitochondrial dysfunction.
- Strategies to improve mitochondrial homeostasis, biogenesis, and turnover show potential for renal protection.
- Modulating mitochondrial function presents promising therapeutic avenues for kidney diseases.
Conclusions:
- Mitochondrial health is critical for preventing kidney damage from oxidative stress.
- Targeting mitochondrial pathways offers a promising strategy for treating and preventing kidney diseases.
- Further research into mitochondria-targeted therapies could lead to novel treatments for renal failure.
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