ArticleCell death & disease2019
Ets-1 deficiency alleviates nonalcoholic steatohepatitis via weakening TGF-β1 signaling-mediated hepatocyte apoptosis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- A data-driven framework reconstructs the molecular continuum of human MASLD progression.Nature metabolism · 2026Article
- Integrative analyses elucidate transcriptional regulatory functions of risk alleles for metabolic liver disease.Nature genetics · 2026Article
- ETS1 suppresses hepatic stellate cell activation and liver fibrosis.JCI insight · 2025Article
- Comprehensive map of the regulatory network triggered by MET exon 14 skipping reveals important involvement of the RAS-ERK signaling pathway.Cell death & disease · 2025Article
- Role of the E26 transformation specific transcription factor family in metabolic disorders.Journal of endocrinological investigation · 2025Review
- Integrative functional genomics reveals transcriptional regulatory function of risk alleles for metabolic liver disease.Research square · 2025Article
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Killing hepatocellular carcinoma in the NAFLD/NASH stage: a comprehensive perspective on targeting regulated cell death.Cell death discovery · 2025Review
- Salsalate improves the anti-tumor efficacy of lenvatinib in MASH-driven hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Exosomal miR-499a-5p from human umbilical cord mesenchymal stem cells attenuates liver fibrosis via targeting ETS1/GPX4-mediated ferroptosis in hepatic stellate cells.Journal of nanobiotechnology · 2025Article
- Inhibiting de novo lipogenesis identifies a therapeutic vulnerability in therapy-resistant colorectal cancer.Redox biology · 2025Article
- Chemogenomic Screening in a Patient-Derived 3D Fatty Liver Disease Model Reveals the CHRM1-TRPM8 Axis as a Novel Module for Targeted Intervention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Xanthohumol overcomes osimertinib resistance via governing ubiquitination-modulated Ets-1 turnover.Cell death discovery · 2024Article
- Effective roles of exercise and diet adherence in non-alcoholic fatty liver disease.World journal of gastroenterology · 2024Article
- M2 macrophages independently promote beige adipogenesis via blocking adipocyte Ets1.Nature communications · 2024Article
- Ubiquitination and Metabolic Disease.Advances in experimental medicine and biology · 2024Review
- Found in translation-Fibrosis in metabolic dysfunction-associated steatohepatitis (MASH).Science translational medicine · 2023Review
- Dysregulation of murine long noncoding single-cell transcriptome in nonalcoholic steatohepatitis and liver fibrosis.RNA (New York, N.Y.) · 2023Article
- The roles of ETS transcription factors in liver fibrosis.Human cell · 2023Review
- Integrative network-based analysis on multiple Gene Expression Omnibus datasets identifies novel immune molecular markers implicated in non-alcoholic steatohepatitis.Frontiers in endocrinology · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
Hepatocyte apoptosis is a hallmark of nonalcoholic steatohepatitis (NASH) and contributes to liver injury, fibrosis, and inflammation. However, the molecular mechanisms underlying excessive hepatocyte apoptosis in NASH remain largely unknown. This study aimed to explore whether and how the v-ets avian erythroblastosis virus E26 oncogene homolog 1 (Ets-1) is involved in diet-induced hepatocyte apoptosis in mice. The study found that the expression level of hepatic Ets-1 was elevated in a NASH mouse model as a result of the activation of transforming growth factor beta1 (TGF-β1) signaling. In the presence of TGF-β1, phosphorylated mothers against decapentaplegic homolog 2/3 (p-Smad2/3) translocated to the binding sites of the Ets-1 promoter to upregulate the expression of Ets-1 in primary hepatocytes. In addition, Ets-1 bound directly to phosphorylated Smad3 (p-Smad3), thereby preventing the ubiquitination and proteasomal degradation of p-Smad3 and enhancing the activity of TGF-β1/Smad3 signaling. Consequently, elevated Ets-1 stimulated TGF-β1-induced hepatocyte apoptosis. However, Ets-1 knockdown alleviated diet-induced hepatocyte apoptosis and NASH with reduced liver injury, inflammation, and fibrosis. Taken together, Ets-1 had an adverse impact on hepatocyte survival under TGF-β1 treatment and accelerated the development of NASH in mice.
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