ArticleAnnals of translational medicine2021
ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevation of GPX4 expression and lipid accumulation.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Ambrisentan Exhibits Hepatoprotective Effects Against NASH-Associated Hepatic Injury in Dexamethasone-Treated Rats Through Regulation of Inflammation, Ferroptosis and Autophagy.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Empagliflozin attenuates dexamethasone-induced non-alcoholic steatohepatitis by regulation of ferroptosis, inflammation and autophagy.Frontiers in pharmacology · 2026Article
- Involvement of ferroptosis in metabolic dysfunction-associated steatohepatitis-related liver diseases.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Innovative approaches to metabolic dysfunction-associated steatohepatitis diagnosis and stratification.Non-coding RNA research · 2025Article
- Identification of Ferroptosis -Related Genes in MAFLD/MASH and HQHF Validation.Hepatic medicine : evidence and research · 2025Article
- Development of a diagnostic model for MASLD and identification of daidzein as the potential drug using bioinformatics analysis and experiments.Frontiers in immunology · 2025Article
- A prognostic molecular signature of hepatic steatosis is spatially heterogeneous and dynamic in human liver.Cell reports. Medicine · 2024Article
- A Scoping Review on Hepatoprotective Mechanism of Herbal Preparations through Gut Microbiota Modulation.Current issues in molecular biology · 2024Article
- Ferroptosis: principles and significance in health and disease.Journal of hematology & oncology · 2024Review
- Article
- Chronic Aroclor 1260 exposure alters the mouse liver proteome, selenoproteins, and metals in steatotic liver disease.Environmental toxicology and pharmacology · 2024Article
- [Research progress on the mechanism of action of heme oxygenase-1 regulating ferroptosis in non-alcoholic fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2024Review
- Identification and validation of cuproptosis-related molecular clusters in non-alcoholic fatty liver disease.Journal of cellular and molecular medicine · 2024Article
- Ferroptosis at the nexus of metabolism and metabolic diseases.Theranostics · 2024Review
- Secreted folate receptor γ drives fibrogenesis in metabolic dysfunction-associated steatohepatitis by amplifying TGFβ signaling in hepatic stellate cells.Science translational medicine · 2023Article
- Zooming in and out of ferroptosis in human disease.Frontiers of medicine · 2023Review
- Iron as a therapeutic target in chronic liver disease.World journal of gastroenterology · 2023Review
- Machine learning identifies ferroptosis-related gene ANXA2 as potential diagnostic biomarkers for NAFLD.Frontiers in endocrinology · 2023Article
- Use of a ferroptosis-related gene signature to construct diagnostic and prognostic models for assessing immune infiltration in metabolic dysfunction-associated fatty liver disease.Frontiers in cell and developmental biology · 2023Article
- Pathological Connections between Nonalcoholic Fatty Liver Disease and Chronic Kidney Disease.Kidney diseases (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundENO3 expression is upregulated in Non-alcoholic fatty liver disease (NAFLD) patient tissues, demonstrated that ENO3 might play crucial roles in NAFLD. However, the mechanism of ENO3 in NAFLD remains unclear. Therefore, this study aimed to investigate the regulatory mechanism of ENO3 in the progression of non-alcoholic steatohepatitis (NASH)
methods
resultsNASH mouse model was successfully established induced by MCD diet with steatosis, inflammatory infiltration, ballooning and fibrosis observed in the liver tissue. The expression of ENO3 and GPX4 was significantly elevated while ferroptosis was inhibited in NASH mice and cell model. Upregulation of both ENO3 and GPX4 could promote the lipid accumulation in L02 cells. In addition, overexpressed ENO3 attenuated the status of ferroptosis.
conclusionsIn the present study, we demonstrate that ENO3 promoted the progression of NASH by negatively regulating ferroptosis via elevating GPX4 expression and lipid accumulation. These findings provided solid foundation for the mechanism of ferroptosis on the progression of NASH regulated by ENO3, suggesting that ENO3 may be a potential therapeutic target for NASH.
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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 Socratic graph.