ArticlePloS one2012
Role of mitofusin 2 in the renal stress response.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Maqui and Chronic Kidney Disease: A Narrative Review on the Potential Nephroprotective Role of Anthocyanins.Nutrients · 2025Review
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- Omega-3 Fatty Acids Modify Drp1 Expression and Activate the PINK1-Dependent Mitophagy Pathway in the Kidney and Heart of Adenine-Induced Uremic Rats.Biomedicines · 2024Article
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Increased Ca2 + transport across the mitochondria-associated membranes by Mfn2 inhibiting endoplasmic reticulum stress in ischemia/reperfusion kidney injury.Scientific reports · 2023Article
- Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.American journal of physiology. Renal physiology · 2023Review
- Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023Review
- Gene signature and prediction model of the mitophagy-associated immune microenvironment in renal ischemia-reperfusion injury.Frontiers in immunology · 2023Article
- Review
- Mitochondria as mediators of systemic inflammation and organ cross talk in acute kidney injury.American journal of physiology. Renal physiology · 2022Review
- Conditional deletion of myeloid-specific mitofusin 2 but not mitofusin 1 promotes kidney fibrosis.Kidney international · 2022Article
- Regulation of Mitochondrial Homeostasis and Nrf2 in Kidney Disease: Timing Is Critical.Oxidative medicine and cellular longevity · 2022Review
- Combination of Perindopril Erbumine and Huangqi-Danshen Decoction Protects Against Chronic Kidney Disease via Sirtuin3/Mitochondrial Dynamics Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The role of metabolic reprogramming in tubular epithelial cells during the progression of acute kidney injury.Cellular and molecular life sciences : CMLS · 2021Review
- Mesenchymal stem cell-derived microvesicles improve intestinal barrier function by restoring mitochondrial dynamic balance in sepsis rats.Stem cell research & therapy · 2021Article
- Mitochondrial quality control in kidney injury and repair.Nature reviews. Nephrology · 2021Review
- Melatonin Improves Mitochondrial Dynamics and Function in the Kidney of Zücker Diabetic Fatty Rats.Journal of clinical medicine · 2020Article
- The Emerging Role of Mitophagy in Kidney Diseases.Journal of life sciences (Westlake Village, Calif.) · 2019Article
- Mitochondrial dynamics and their potential as a therapeutic target.Mitochondrion · 2019Review
- Mesenchymal stem cell therapy targeting mitochondrial dysfunction in acute kidney injury.Journal of translational medicine · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The role of mitofusin 2 (MFN2), a key regulator of mitochondrial morphology and function in the renal stress response is unknown. To assess its role, the MFN2 floxed gene was conditionally deleted in the kidney of mice (MFN2 cKO) by Pax2 promoter driven Cre expression (Pax2Cre). MFN2 cKO caused severe mitochondrial fragmentation in renal epithelial cells that are critical for normal kidney tubular function. However, despite a small (20%) decrease in nephron number, newborn cKO pups had organ or tubular function that did not differ from littermate Cre-negative pups. MFN2 deficiency in proximal tubule epithelial cells in primary culture induced mitochondrial fragmentation but did not significantly alter ATP turnover, maximal mitochondrial oxidative reserve capacity, or the low level of oxygen consumption during cyanide exposure. MFN2 deficiency also did not increase apoptosis of tubule epithelial cells under non-stress conditions. In contrast, metabolic stress caused by ATP depletion exacerbated mitochondrial outer membrane injury and increased apoptosis by 80% in MFN2 deficient vs. control cells. Despite similar stress-induced Bax 6A7 epitope exposure in MFN2 deficient and control cells, MFN2 deficiency significantly increased mitochondrial Bax accumulation and was associated with greater release of both apoptosis inducing factor and cytochrome c. In conclusion, MFN2 deficiency in the kidney causes mitochondrial fragmentation but does not affect kidney or tubular function during development or under non-stress conditions. However, MFN2 deficiency exacerbates renal epithelial cell injury by promoting Bax-mediated mitochondrial outer membrane injury and apoptosis.
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