ArticleJournal of the American Society of Nephrology : JASN2015
Conditional knockout of proximal tubule mitofusin 2 accelerates recovery and improves survival after renal ischemia.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- The role of mitochondria in the gut-kidney axis: implications for kidney health.Frontiers in pharmacology · 2026Review
- Mitochondrial calcium uniporter-mediated mitochondrial dynamics imbalance contributes to contrast medium-induced renal tubular cell injury.Frontiers in molecular biosciences · 2026Article
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- A mitochondrial regulator protein, mitofusin 2, is elevated in the maternal blood of women with preeclampsia.BMC pregnancy and childbirth · 2025Article
- Twist2 knockdown alleviates renal ischemia-reperfusion injury by maintaining mitochondrial function and enhancing mitophagy through Bnip3.Human cell · 2025Article
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- The role of mitochondrial dynamics in disease.MedComm · 2023Review
- Autophagy and mitophagy: physiological implications in kidney inflammation and diseases.American journal of physiology. Renal physiology · 2023Review
- Metabolic reprogramming heterogeneity in chronic kidney disease.FEBS open bio · 2023Review
- Mitochondrial quality control in acute kidney disease.Journal of nephrology · 2023Review
- Mitofusin-2 mediates cannabidiol-induced neuroprotection against cerebral ischemia in rats.Acta pharmacologica Sinica · 2023Article
- Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- The multifaceted role of kidney tubule mitochondrial dysfunction in kidney disease development.Trends in cell biology · 2022Review
- Conditional deletion of myeloid-specific mitofusin 2 but not mitofusin 1 promotes kidney fibrosis.Kidney international · 2022Article
- Article
- Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022Review
- In vivo evidence for therapeutic applications of beclin 1 to promote recovery and inhibit fibrosis after acute kidney injury.Kidney international · 2022Article
- Mitochondrial quality control in kidney injury and repair.Nature reviews. Nephrology · 2021Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Proximal tubule (PT) cells are critical targets of acute ischemic injury. Elimination of the mitochondrial fusion protein mitofusin 2 (Mfn2) sensitizes PT cells to apoptosis in vitro. However, the role of PT Mfn2 in ischemic AKI in vivo is unknown. To test its role, we evaluated the effects of conditional KO of PT Mfn2 (cKO-PT-Mfn2) on animal survival after transient bilateral renal ischemia associated with severe AKI. Forty-eight hours after ischemia, 28% of control mice survived compared with 86% of cKO-PT-Mfn2 animals (P<0.001 versus control). Although no significant differences in histologic injury score, apoptosis, or necrosis were detected between genotypes, cKO-PT-Mfn2 kidneys exhibited a 3.5-fold increase in cell proliferation restricted to the intrarenal region with Mfn2 deletion. To identify the signals responsible for increased proliferation, primary PT cells with Mfn2 deficiency were subjected to stress by ATP depletion in vitro. Compared with normal Mfn2 expression, Mfn2 deficiency significantly increased PT cell proliferation and persistently activated extracellular signal-regulated kinase 1/2 (ERK1/2) during recovery from stress. Furthermore, stress and Mfn2 deficiency decreased the interaction between Mfn2 and Ras detected by immunoprecipitation, and purified Mfn2 dose-dependently decreased Ras activity in a cell-free assay. Ischemia in vivo also reduced the Mfn2-RAS interaction and increased both RAS and p-ERK1/2 activity in the renal cortical homogenates of cKO-PT-Mfn2 mice. Our results suggest that, in contrast to its proapoptotic effects in vitro, selective PT Mfn2 deficiency accelerates recovery of renal function and enhances animal survival after ischemic AKI in vivo, partly by increasing Ras-ERK-mediated cell proliferation.
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