ArticleAutophagy2018
PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury.
Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
182 citing papers in PubMed, 1 synthesis or guideline pooled it, 290 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
- Mitophagy in cisplatin-induced kidney injury: regulatory mechanisms and therapeutic targets.Annals of medicine · 2026Review
- Curcumin regulates ferroptosis by activating α7 nicotinic acetylcholine receptor to improve sepsis-induced acute kidney injury.Renal failure · 2026Article
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- Flow Cytometry and AI-Driven Biomarker Discovery in Acute Kidney Injury: From Mechanistic Insights to Translation Applications in Clinical and Austere Environments.International journal of molecular sciences · 2026Review
- Layered double hydroxide nanocarriers loaded with butylphthalide attenuate the AKI-CKD transition by regulating mitophagy.Materials today. Bio · 2026Article
- PRKCD Orchestrates Sevoflurane-Induced Cognitive Dysfunction in Aged Rats by Regulating PINK1/PRKN Mitophagy Pathway.Journal of cellular and molecular medicine · 2026Article
- Review
- Review
- HIF-1α-mediated mitochondrial autophagy in the post-treatment protective effect of thyroxine against myocardial ischemia-reperfusion injury.Journal of cardiothoracic surgery · 2026Article
- Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026Article
- Overcoming Oxidative Stress in Parkinson's Disease: NADPH Oxidase 4 (NOX4) as a Potential Therapeutic Target.Antioxidants (Basel, Switzerland) · 2026Review
- LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy.Chinese medical journal · 2026Article
- RPS3 Aggravates Sepsis-Induced Acute Kidney Injury Through Activating NF-kappaB Mediated Renal Inflammatory Responses.Physiological research · 2026Article
- Mitophagy in kidney transplantation ischemia-reperfusion injury.International urology and nephrology · 2026Review
- Defective autophagy and AMPK inactivation drive ferroptosis in diabetic kidney disease.Diabetologia · 2026Article
- Mitigation of Ischemia/Reperfusion-Induced Acute Kidney Injury by Canagliflozin Is Associated with Altered Mitochondrial Dynamics and Reduced Proliferation in Swine.Biomolecules · 2026Article
- Autophagy-lysosome flux failure in diabetic kidney disease: tubular vulnerability and cell-state remodeling.Frontiers in endocrinology · 2026Review
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Autophagy in kidney physiology: from cellular quality control to organ metabolism.Autophagy reports · 2026Review
122 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damaged or dysfunctional mitochondria are toxic to the cell by producing reactive oxygen species and releasing cell death factors. Therefore, timely removal of these organelles is critical to cellular homeostasis and viability. Mitophagy is the mechanism of selective degradation of mitochondria via autophagy. The significance of mitophagy in kidney diseases, including ischemic acute kidney injury (AKI), has yet to be established, and the involved pathway of mitophagy remains poorly understood. Here, we show that mitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI. Mitophagy under these conditions is abrogated by Pink1 and Park2 deficiency, supporting a critical role of the PINK1-PARK2 pathway in tubular cell mitophagy. Moreover, ischemic AKI is aggravated in pink1 andpark2 single- as well as double-knockout mice. Mechanistically, Pink1 and Park2 deficiency enhances mitochondrial damage, reactive oxygen species production, and inflammatory response. Taken together, these results indicate that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function 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.