Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease
Open accessAbstract
The kidney contains many mitochondria that generate ATP to provide energy for cellular processes. Oxidative stress injury can be caused by impaired mitochondria with excessive levels of reactive oxygen species. Accumulating evidence has indicated a relationship between oxidative stress and kidney diseases, and revealed new insights into mitochondria-targeted therapeutics for renal injury. Improving mitochondrial homeostasis, increasing mitochondrial biogenesis, and balancing mitochondrial turnover has the potential to protect renal function against oxidative stress. Although there are some reviews that addressed this issue, the articles summarizing the relationship between mitochondria-targeted effects and the risk factors of renal failure are still few. In this review, we integrate recent studies on oxidative stress and mitochondrial function in kidney diseases, especially chronic kidney disease. We organized the causes and risk factors of oxidative stress in the kidneys based in their mitochondria-targeted effects. This review also listed the possible candidates for clinical therapeutics of kidney diseases by modulating mitochondrial function.
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MGF has renoprotective effects across kidney injury models by modulating inflammation, oxidative stress, and fibrotic signaling pathways.
“MGF has demonstrated renoprotective effects across a range of kidney injury models by modulating inflammation, oxidative stress and fibrotic signaling pathways (140).”
From Mangiferin in human disease: Multifaceted mechanisms and applications (Review) (2026) · cites this paper as [140]
Section 2.4 discusses renal protection by curcumin and other compounds, but does not identify MGF or attribute these effects to it. Searches for “MGF” and “mangiferin” found no passage in our copy addressing MGF’s effects across kidney injury models or the claimed pathways. (LLM, conf=0.76)
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Mangiferin in human disease: Multifaceted mechanisms and applications (Review)
Dai, Y., Huang, Q., Tan, M., Wang, Z., Jiang, C., Liu, Z., Zhang, S., & Song, S. (2026) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2026.5736 · Cited by 3 · see citing works
“MGF has demonstrated renoprotective effects across a range of kidney injury models by modulating inflammation, oxidative stress and fibrotic signaling pathways (140).”
- Authors
- Ho, H.-J., & Shirakawa, H.
- Affiliations
- Hokkaido University (JP)
- Tohoku University (JP)
- Corresponding author
- Ho, Hsin-Jung
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2022-12-25
- Volume
- 12
- Issue
- 1
- Pages
- 88
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC9818928
- OpenAlex
- W4312205820
- Cited by
- 255
- References
- 9
- Citations by year
- 2026: 78 · 2025: 91 · 2024: 65 · 2023: 21
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (JSPS) (#22K1174602)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- oxidative stress, mitochondrial dysfunction, chronic kidney disease, reactive oxygen species, mitochondrial biogenesis, mitochondrial turnover, mitochondrial homeostasis, kidney injury
- MeSH terms
- Humans, Kidney, Mitochondria, Reactive Oxygen Species, Oxidative Stress, Renal Insufficiency, Chronic
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