ArticleRedox biology2019
Mst1 inhibition attenuates non-alcoholic fatty liver disease via reversing Parkin-related mitophagy.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed.
- ZNF143 suppresses mitophagy to drive MASLD progression by regulating SMURF1/TRPV1 axis.Molecular genetics and genomics : MGG · 2026Article
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- Profiling of extracellular vesicles from primary hepatocytes, organoids, and mash patients identifies cell injury-specific signatures.Scientific reports · 2026Article
- Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review.Proteomes · 2026Review
- Metabolic profiling of steatotic liver disease by fluorescence lifetime imaging microscopy.Communications medicine · 2026Article
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- Mitochondrial Calcium Signaling in Hepatocyte Health and Disease.Cold Spring Harbor perspectives in biology · 2026Review
- NRAS and SREBF1 identified as mitophagy-associated risk genes for rheumatoid arthritis through interpretable machine learning and experimental validation studies.BMC rheumatology · 2026Article
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- NEDD4L knockdown reduced lipid accumulation in non-alcoholic fatty liver disease by promoting the activity of PI3K/AKT signaling pathway.European journal of medical research · 2025Article
- Circadian disruption aggravates non-alcoholic fatty liver disease by activating RIPK1-RIPK3-MLKL axis in mice.Scientific reports · 2025Article
- AMPK affects the development of early-stage NAFLD by activating autophagy and fatty acid oxidation.Scientific reports · 2025Article
- Mitophagy as a pivotal axis in non‑alcoholic fatty liver disease: From pathogenic mechanisms to therapeutic strategies (Review).Molecular medicine reports · 2025Review
- Article
- L-Phenylalanine promotes liver steatosis by inhibiting BNIP3-mediated mitophagy.Molecular medicine (Cambridge, Mass.) · 2025Article
- High fat diet (HFD) induced hepatic lipogenic metabolism and lipotoxicity via Parkin-dependent mitophagy and Errα signal of Pelteobagrus fulvidraco.Journal of animal science and biotechnology · 2025Article
- Impaired Mitophagy Contributes to Pyroptosis in Sarcopenic Obesity Zebrafish Skeletal Muscle.Nutrients · 2025Article
- Mitochondrial Dysfunction as a Pathogenesis and Therapeutic Strategy for Metabolic-Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- Mitochondria at the Crossroads: Linking the Mediterranean Diet to Metabolic Health and Non-Pharmacological Approaches to NAFLD.Nutrients · 2025Review
- Flutamide Promotes Early Hepatocarcinogenesis Through Mitophagy in High-Fat Diet-Fed Non-Obese Steatotic Rats.International journal of molecular sciences · 2025Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity-related non-alcoholic fatty liver disease (NAFLD) is connected with mitochondrial stress and hepatocyte apoptosis. Parkin-related mitophagy sustains mitochondrial homeostasis and hepatocyte viability. However, the contribution and regulatory mechanisms of Parkin-related mitophagy in NAFLD are incompletely understood. Macrophage stimulating 1 (Mst1) is a novel mitophagy upstream regulator which excerbates heart and cancer apoptosisn via repressing mitophagy activity. The aim of our study is to explore whether Mst1 contributes to NAFLD via disrupting Parkin-related mitophagy. A NAFLD model was generated in wild-type (WT) mice and Mst1 knockout (Mst1-KO) mice using high-fat diet (HFD). Cell experiments were conducted via palmitic acid (PA) treatment in the primary hepatocytes. The results in our study demonstrated that Mst1 was significantly upregulated in HFD-treated livers. Genetic ablation of Mst1 attenuated HFD-mediated hepatic injury and sustained hepatocyte viability. Functional studies illustrated that Mst1 knockdown reversed Parkin-related mitophagy and the latter protected mitochondria and hepatocytes against HFD challenge. Besides, we further figured out that Mst1 modulated Parkin expression via the AMPK pathway; blockade of AMPK repressed Parkin-related mitophagy and recalled hepatocytes mitochondrial apoptosis. Altogether, our data identified that NAFLD was closely associated with the defective Parkin-related mitophagy due to Mst1 upregulation. This finding may pave the road to new therapeutic modalities for the treatment of fatty liver disease.
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