ArticleBritish journal of pharmacology2020
Cyanidin-3-O-glucoside improves non-alcoholic fatty liver disease by promoting PINK1-mediated mitophagy in mice.
Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
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Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Effects of anthocyanin supplementation on blood lipid levels: a systematic review and meta-analysis.Frontiers in nutrition · 2023Pooled it
- ZNF143 suppresses mitophagy to drive MASLD progression by regulating SMURF1/TRPV1 axis.Molecular genetics and genomics : MGG · 2026Article
- Polyphenols as Systems Modulators of the Gut-Brain-Liver Axis: A Narrative Review of Neuro-Metabolic and Immunomodulatory Networks.Molecular nutrition & food research · 2026Review
- Jabuticaba (Pharmaceuticals (Basel, Switzerland) · 2026Article
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Lycopene Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease via PINK1/Parkin-Mediated Mitophagy Activation and Apoptosis Attenuation.Antioxidants (Basel, Switzerland) · 2026Article
- Cyanidin-3-O-galactoside Attenuates Metabolic Dysfunction-associated Steatotic Liver Disease by Modulating the CCL3-FABP4 Axis.Plant foods for human nutrition (Dordrecht, Netherlands) · 2026Article
- Enzymatic Modification of Flavonoids: Implications for Bioavailability, Bioactivity, and Therapeutic Potential Based on a Systematic Review and Bioinformatics Analysis.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting the Gut-Liver Mitochondria Axis in MASLD: Mechanisms and Therapeutic Perspectives.Current medical science · 2026Review
- Cyanidin-3,5-O-Glucoside Alleviates DSS-Induced Colon Barrier Dysfunction and Fibrosis Through Autophagy-Associated Pathway-Mediated Inflammation Repression in a C57BL/6J Mouse Model.Applied biochemistry and biotechnology · 2026Article
- Salidroside alleviates palmitic acid-induced hepatocyte injury by regulating the LILRB2-mediated autophagy pathway.In vitro cellular & developmental biology. Animal · 2026Article
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
- The therapeutic potential of botanicals: how medicinal plants targeting autophagy can reverse metabolic-associated fatty liver disease.Frontiers in pharmacology · 2026Review
- Mitophagy as a pivotal axis in non‑alcoholic fatty liver disease: From pathogenic mechanisms to therapeutic strategies (Review).Molecular medicine reports · 2025Review
- Review
- Blueberry Anthocyanins Ameliorate Hepatic Dysfunction in High-Fat Diet-Fed Mice: Association with Altered Gut Microbiota and Bile Acid Metabolism.Foods (Basel, Switzerland) · 2025Article
- Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025Review
- Induction of Autophagy as a Therapeutic Breakthrough for NAFLD: Current Evidence and Perspectives.Biology · 2025Review
- Research Progress and Prospects of Flavonoids in the Treatment of Hyperlipidemia: A Narrative Review.Molecules (Basel, Switzerland) · 2025Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
background and purposeIdentifying safe and effective compounds that target to mitophagy to eliminate impaired mitochondria may be an attractive therapeutic strategy for non-alcoholic fatty liver disease. Here, we investigated the effects of cyanidin-3-O-glucoside (C3G) on non-alcoholic fatty liver disease (NAFLD) and the underlying mechanism. EXPERIMENTAL APPROACH: Non-alcoholic fatty liver disease was induced by a high-fat diet for 16 weeks. C3G was administered during the last 4 weeks. In vivo, recombinant adenoviruses and AAV8 were used for overexpression and knockdown of PTEN-induced kinase 1 (PINK1), respectively. AML-12 and HepG2 cells were used for the mechanism study. KEY
resultsC3G administration suppressed hepatic oxidative stress, NLR family pyrin domain containing 3 (NLRP3) inflammasome activation and steatosis and improved systemic glucose metabolism in mice with NAFLD. These effects of C3G were also observed in palmitic acid-treated AML-12 cells and hepatocytes from NAFLD patients. Mechanistic investigations revealed that C3G increased PINK1/Parkin expression and mitochondrial localization and promoted PINK1-mediated mitophagy to clear damaged mitochondria. Knockdown of hepatic PINK1 abolished the mitophagy-inducing effect of C3G, which blunted the beneficial effects of C3G on oxidative stress, NLRP3 inflammasome activation, hepatic steatosis and glucose metabolism. CONCLUSION AND IMPLICATIONS: These results demonstrate that PINK1-mediated mitophagy plays an essential role in the ability of C3G to alleviate NAFLD and suggest that C3G may be a potential drug candidate for NAFLD treatment.
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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.