ArticleJournal of translational medicine2020
Role of Parkin-mediated mitophagy in the protective effect of polydatin in sepsis-induced acute kidney injury.
Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- Polydatin Delivery Systems and Nanomedicine: Pharmacology, Preclinical Evidence, and Translation.Pharmaceutics · 2026Review
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Epigenetics-mediated pathological alterations and their diagnostic and therapeutic potential in sepsis-associated acute kidney injury.Clinical epigenetics · 2026Review
- TREM1-NLRP3-driven pyroptosis in sepsis-associated acute kidney injury (AKI) with parallel autophagy changes.Scientific reports · 2026Article
- Role of mitophagy in acute and fractionated gamma radiation-induced nephropathy in rats: insight into molecular biology and repurposing of rosuvastatin.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bidirectional Regulation of NLRP3 Inflammasome and Mitochondrial Quality Control in Sepsis: Mechanisms and Therapeutic Implications.Mediators of inflammation · 2026Review
- Tanshinone IIA prevents septicemia acute kidney injury via regulating the DUSP10/JNK/P38/NLRP3 pathway.American journal of translational research · 2026Article
- Mitochondrial Dysfunction in Cardiac Diseases: Insights into Pathophysiology and Clinical Outcomes.Current cardiology reviews · 2026Review
- Improved bioavailability and anti-nephrotoxicity efficacy of polydatin on cisplatin-induced AKIInternational journal of pharmaceutics: X · 2025Article
- Research Progress on Signalling Pathways Related to Sepsis-Associated Acute Kidney Injury in Children.Current issues in molecular biology · 2025Review
- Potential of Polydatin Against Ischemia-Reperfusion Injury: New Insights from Pharmacological-Pathological Mechanism Associations.Drug design, development and therapy · 2025Review
- The Role of Mitochondrial Dysfunction in Sepsis-Associated Acute Kidney Injury: A Narrative Review.Drug design, development and therapy · 2025Review
- Histone deacetylases: potential therapeutic targets in cisplatin-induced acute kidney injury.Annals of medicine · 2024Review
- Mitochondrial dysfunction in acute kidney injury.Renal failure · 2024Review
- αKlotho modulates BNIP3-mediated mitophagy by regulating FoxO3 to decrease mitochondrial ROS and apoptosis in contrast-induced acute kidney injury.Cellular and molecular life sciences : CMLS · 2024Article
- Pharmacological Activation and Transgenic Overexpression of SIRT1 Attenuate Traumatic Optic Neuropathy Induced by Blunt Head Impact.Translational vision science & technology · 2024Article
- Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024Review
- Article
- Pharmacological Potential of Kaempferol, a Flavonoid in the Management of Pathogenesis via Modulation of Inflammation and Other Biological Activities.Molecules (Basel, Switzerland) · 2024Review
- Sepsis-Associated Acute Kidney Injury: Where Are We Now?Medicina (Kaunas, Lithuania) · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe have reported that polydatin (PD) alleviates mitochondrial dysfunction in rat models of sepsis-induced acute kidney injury (SI-AKI), but the mechanism is not well understood. Here, we investigated the role of Parkin-mediated mitophagy in the protective effects of PD in SI-AKI in mice.
methodsSepsis was induced in the mice by caecal ligation and puncture. Mitophagy was determined by mitochondrial mass. NLRP3 inflammasome activation was determined by NLRP3, ASC and caspase-1. Mitophagy was blocked by treatment with mitochondrial division inhibitor-1 and Parkin knockout. KEY
resultsPD treatment increased the sepsis-induced loss of mitochondrial mass, indicating the upregulation of mitophagy. Furthermore, PD treatment mediated Parkin translocation from the cytoplasm to the mitochondria. This suggests that Parkin-mediated mitophagy is an underlying mechanism. This was confirmed by the suppression of PD-induced mitophagy in Parkin-/- mice and in mice that were treated with a mitophagy inhibitor. PD-induced Parkin translocation and mitophagy were blocked by inhibiting SIRT1; thus, activation of SIRT1 might be an important molecular mechanism that is triggered by PD. Additionally, PD treatment protected against sepsis-induced kidney injury. These effects were blocked by inhibition of Parkin-dependent mitophagy. Furthermore, PD also protected against mitochondrial dysfunction and mitochondria-dependent apoptosis, and the effect was blocked when Parkin-dependent mitophagy was inhibited. Finally, PD suppressed NLRP3 inflammasome activation that was also dependent on Parkin-mediated mitophagy.
conclusionsThese findings indicate that Parkin-mediated mitophagy is important for the protective effect of PD in SI-AKI, and the underlying mechanisms include the inhibition of mitochondrial dysfunction and NLRP3 inflammasome activation.
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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.