ArticleRedox biology2021
The PINK1/PARK2/optineurin pathway of mitophagy is activated for protection in septic acute kidney injury.
Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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Who cites it
107 citing papers in PubMed, 184 citations in OpenAlex.
- Insights from integrative spatial transcriptomics in sepsis-associated acute kidney injury.Nature reviews. Nephrology · 2026Review
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Article
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Zinc regulates the balance of specific gut microbiota through MTF1/Nrf2 and mitigates ferroptosis through activation of PINK1/Parkin/mitophagy via the gut-kidney axis in sepsis-associated acute kidney injury in pregnant mice.Apoptosis : an international journal on programmed cell death · 2026Article
- Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026Article
- Article
- TREM1-NLRP3-driven pyroptosis in sepsis-associated acute kidney injury (AKI) with parallel autophagy changes.Scientific reports · 2026Article
- Renoprotection by 5-Methoxytryptophan in Kidney Disease.Biomolecules · 2026Review
- Naringenin-functionalized polyester nanoparticles improve oral urolithin A delivery and protect against cisplatin-induced kidney injury via heme oxygenase-1 activation and mitochondrial quality control.The Journal of pharmacology and experimental therapeutics · 2026Article
- Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome.Journal of inflammation research · 2026Review
- MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy.Frontiers in pediatrics · 2026Article
- Article
- Autophagy-lysosome flux failure in diabetic kidney disease: tubular vulnerability and cell-state remodeling.Frontiers in endocrinology · 2026Review
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- Molecular hydrogen-mediated SIRT1 activation alleviates sepsis-associated encephalopathy by promoting mitophagy.European journal of medical research · 2025Article
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- Vitamin D receptor modulates autophagy via miR-20a-5p/ATG16L1 axis to alleviate lipopolysaccharide-induced acute kidney injury.Renal failure · 2025Article
- Xuebijing injection alleviates septic acute kidney injury by modulating inflammation, mitochondrial dysfunction, and endoplasmic reticulum stress.Renal failure · 2025Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is the major cause of acute kidney injury (AKI) associated with high mortality rates. Mitochondrial dysfunction contributes to the pathophysiology of septic AKI. Mitophagy is an important mitochondrial quality control mechanism that selectively eliminates damaged mitochondria, but its role and regulation in septic AKI remain largely unknown. Here, we demonstrate the induction of mitophagy in mouse models of septic AKI induced by lipopolysaccharide (LPS) treatment or by cecal ligation and puncture. Mitophagy was also induced in cultured proximal tubular epithelial cells exposed to LPS. Induction of mitophagy under these experimental setting was suppressed by pink1 or park2 knockout, indicating the role of the PINK1/PARK2 pathway of mitophagy in septic AKI. In addition, sepsis induced more severe kidney injury and cell apoptosis in pink1 or park2 knockout mice than in wild-type mice, suggesting a beneficial role of mitophagy in septic AKI. Furthermore, in cultured renal tubular cells treated with LPS, knockdown of pink1 or park2 inhibited mitochondrial accumulation of the autophagy adaptor optineurin (OPTN) and silencing Optn inhibited LPS-induced mitophagy. Taken together, these findings suggest that the PINK1/PARK2 pathway of mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function in septic AKI.
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