ArticleCell death & disease2019
Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
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Who cites it
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 212 citations in OpenAlex.
- Current perspectives and trends on the role of mitochondria in renal ischemia-reperfusion injury from 2005 to 2024: a bibliometric analysis and literature review.Frontiers in physiology · 2025Pooled it
- RIPC Protects Against Renal Ischaemia-Reperfusion Injury by Activating SIRT3/Parkin-Mediated Mitophagy.Journal of cellular and molecular medicine · 2026Article
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Article
- Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026Review
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- The role of mitochondria in the gut-kidney axis: implications for kidney health.Frontiers in pharmacology · 2026Review
- Autophagy-lysosome flux failure in diabetic kidney disease: tubular vulnerability and cell-state remodeling.Frontiers in endocrinology · 2026Review
- PANoptosis-Related Diagnostic Biomarkers in Non-Neovascular Age-Related Macular Degeneration: An Integrative Transcriptomic and Experimental Study.Genetics research · 2026Article
- Restrictive hypertonic saline resuscitation is associated with less intestinal injury after hemorrhagic shock in rats and with coordinated changes in MALAT1, miR-145-5p, and BNIP3 expression.Frontiers in surgery · 2026Article
- Targeting MCL1 by UMI-77 to induce mitophagy alleviates renal tubular epithelial cells injury in acute kidney injury.Scientific reports · 2025Article
- Advances in understanding the role of mitochondria in renal ischemia-reperfusion injury.Clinical and experimental nephrology · 2025Review
- Vitexin enhances mitophagy and improves renal ischemia-reperfusion injury by regulating the p38/MAPK pathway.Renal failure · 2025Article
- HMOX1 interacts with BNIP3 to modulate neuronal ferroptosis after spinal cord ischemia-reperfusion injury via a mitophagy-dependent mechanism.Cell death discovery · 2025Article
- The role of Slfn4 in myocardial infarction: mechanisms and implications.Journal of physiology and biochemistry · 2025Article
- Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis.Molecular and cellular biochemistry · 2025Review
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- The effect of USP17 knockdown on autophagic ferroptosis in gastric cancer by regulating the BNIP3-NCOA4-FTH1 axis.Journal of molecular histology · 2025Article
- Circadian gene BMAL1 ameliorates renal ischaemia-reperfusion injury in diabetic mice by enhancing mitophagy via the HIF-1/BNIP3 pathway.Scientific reports · 2025Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia-reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced OGD-R-induced mitophagy, and potentiated OGD-R-induced cell death. In vivo, Bnip3 knockout worsened renal IR injury, as manifested by more severe renal dysfunction and tissue injury. We further showed that Bnip3 knockout reduced mitophagy, which resulted in the accumulation of damaged mitochondria, increased production of reactive oxygen species, and enhanced cell death and inflammatory response in kidneys following renal IR. Taken together, these findings suggest that BNIP3-mediated mitophagy has a critical role in mitochondrial quality control and tubular cell survival during AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.