ArticleAmerican journal of physiology. Renal physiology2020
miR-214 represses mitofusin-2 to promote renal tubular apoptosis in ischemic acute kidney injury.
Article in American journal of physiology. Renal physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- Oxidative stress and endoplasmic reticulum stress in acute kidney injury: mechanistic crosstalk and therapeutic modulation.Frontiers in medicine · 2026Review
- Biomarkers to Predict Acute Kidney Injury in Patients with Trauma.Medicina (Kaunas, Lithuania) · 2025Observational
- Insights into non-coding RNAS: biogenesis, function and their potential regulatory roles in acute kidney disease and chronic kidney disease.Molecular and cellular biochemistry · 2025Review
- MicroRNA‑17‑5p alleviates sepsis‑related acute kidney injury in mice by modulating inflammation and apoptosis.Molecular medicine reports · 2024Article
- Therapeutic Implication of miRNAs as an Active Regulatory Player in the Management of Pain: A Review.Genes · 2024Review
- Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury.Cell death discovery · 2024Review
- Biomarkers to Predict Multiorgan Distress Syndrome and Acute Kidney Injury in Critically Ill Surgical Patients.Medicina (Kaunas, Lithuania) · 2023Article
- From Physiology to Pathology: The Role of Mitochondria in Acute Kidney Injuries and Chronic Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- MicroRNAs as Biomarkers and Therapeutic Targets for Acute Kidney Injury.Diagnostics (Basel, Switzerland) · 2023Review
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury.Frontiers in cell and developmental biology · 2023Review
- Progress and Challenges of Understanding Cardiorenal Syndrome Type 3.Reviews in cardiovascular medicine · 2023Review
- MicroRNA-10 Family Promotes the Epithelial-to-Mesenchymal Transition in Renal Fibrosis by the PTEN/Akt Pathway.Current issues in molecular biology · 2022Article
- MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022Review
- Blood Biomarkers and Metabolomic Profiling for the Early Diagnosis of Vancomycin-Associated Acute Kidney Injury: A Systematic Review and Meta-Analysis of Experimental Studies.Journal of personalized medicine · 2022Review
- The Role of Circadian Clock Genes in Critical Illness: The Potential Role of Translational Clock Gene Therapies for Targeting Inflammation, Mitochondrial Function, and Muscle Mass in Intensive Care.Journal of biological rhythms · 2022Review
- The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury.Cell death discovery · 2022Review
- Analysis of microRNA Expression after Glutamine Intervention in Acute Renal Ischemia-Reperfusion Injury.Journal of healthcare engineering · 2022Article
- Mesenchymal Stem Cells-Derived Exosomes Ameliorate Ischemia/Reperfusion Induced Acute Kidney Injury in a Porcine Model.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Disruption of mitochondrial dynamics is an important pathogenic event in both acute and chronic kidney diseases, but the underlying mechanism remains poorly understood. Here, we report the regulation of mitofusin-2 (Mfn2; a key mitochondrial fusion protein) by microRNA-214 (miR-214) in renal ischemia-reperfusion that contributes to mitochondrial fragmentation, renal tubular cell death, and ischemic acute kidney injury (AKI). miR-214 was induced, whereas Mfn2 expression was decreased, in mouse ischemic AKI and cultured rat kidney proximal tubular cells (RPTCs) following ATP depletion treatment. Overexpression of miR-214 decreased Mfn2. Conversely, inhibition of miR-214 with anti-miR-214 prevented Mfn2 downregulation in RPTCs following ATP depletion. Anti-miR-214 further ameliorated mitochondrial fragmentation and apoptosis, whereas overexpression of miR-214 increased apoptosis, in ATP-depleted RPTCs. To test regulation in vivo, we established a mouse model with miR-214 specifically deleted from kidney proximal tubular cells (PT-
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