Mitochondrial dysfunction and oxidative stress: Role in chronic kidney disease
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Updated: Aug 12, 2025

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Anjali Srivastava1, Bhawna Tomar2, Divyansh Sharma1
1Division of Toxicology and Experimental Medicine, CSIR-Central Drug Research Institute, Lucknow 226031, India.
Insights
Chronic kidney disease (CKD) involves kidney damage and dysfunction. Mitochondrial dysfunction, characterized by altered shape, oxidative stress, and reduced ATP, is a key factor in CKD progression.
Area of Science:
- Nephrology
- Mitochondrial Biology
- Cellular Pathology
Background:
- Chronic kidney disease (CKD) is a progressive condition characterized by irreversible kidney damage, often leading to end-stage kidney disease (ESKD) and the need for transplantation.
- Mitochondria, abundant in kidney cells, play a critical role in cellular energy production and are susceptible to damage in CKD.
- Mitochondrial dysfunction is a recognized hallmark of kidney injury in CKD, manifesting as structural and functional alterations.
Purpose of the Study:
- To summarize recent advancements and novel insights into the role of mitochondrial remodeling in the progression of chronic kidney disease.
- To highlight the sources of acquired mitochondrial dysfunction in CKD.
- To underscore the importance of understanding mitochondrial biology for developing effective CKD treatments.
Main Methods:
- Review of current scientific literature focusing on mitochondrial dynamics and function in the context of chronic kidney disease.
- Analysis of studies investigating the relationship between kidney inflammation, injury, and mitochondrial alterations.
- Synthesis of findings related to changes in mitochondrial morphology, oxidative stress, biogenesis, and ATP production in CKD.
Main Results:
- CKD is associated with significant alterations in mitochondrial morphology and remodeling within kidney tissues.
- Increased mitochondrial oxidative stress and a decline in ATP generation are common features of mitochondrial dysfunction in CKD.
- These mitochondrial changes are linked to kidney inflammatory responses and overall injury progression.
Conclusions:
- Mitochondrial remodeling and dysfunction are integral to the pathogenesis and advancement of chronic kidney disease.
- Understanding the specific mechanisms of mitochondrial dysfunction in CKD is crucial for identifying therapeutic targets.
- Further research into kidney mitochondrial biology holds promise for developing novel treatment strategies for CKD and preventing its progression to ESKD.
Abstract:
Chronic kidney disease (CKD) is associated with a variety of distinct disease processes that permanently change the function and structure of the kidney across months or years. CKD is characterized as a glomerular filtration defect or proteinuria that lasts longer than three months. In most instances, CKD leads to end-stage kidney disease (ESKD), necessitating kidney transplantation. Mitochondrial dysfunction is a typical response to damage in CKD patients. Despite the abundance of mitochondria in the kidneys, variations in mitochondrial morphological and functional characteristics have been associated with kidney inflammatory responses and injury during CKD. Despite these variations, CKD is frequently used to define some classic signs of mitochondrial dysfunction, including altered mitochondrial shape and remodeling, increased mitochondrial oxidative stress, and a marked decline in mitochondrial biogenesis and ATP generation. With a focus on the most significant developments and novel understandings of the involvement of mitochondrial remodeling in the course of CKD, this article offers a summary of the most recent advances in the sources of procured mitochondrial dysfunction in the advancement of CKD. Understanding mitochondrial biology and function is crucial for developing viable treatment options for CKD.
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