ArticleCell reports2024
Hepatic Snai1 and Snai2 promote liver regeneration and suppress liver fibrosis in mice.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Integrative analyses elucidate transcriptional regulatory functions of risk alleles for metabolic liver disease.Nature genetics · 2026Article
- Integrative Single-Cell and Machine Learning Analysis Identifies an EMT-Associated Prognostic Signature for Papillary Thyroid Cancer.Cancer medicine · 2026Article
- Epithelial-mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy.Frontiers in immunology · 2026Review
- Vaccinia-related kinase 1/snail family transcriptional repressor 1 regulates epithelial-mesenchymal transition and inflammation in proliferative vitreoretinopathy.International journal of ophthalmology · 2026Article
- Liver-specific enhancers evolved from independent episodes of MITE domestication in Xenopus tropicalis.Mobile DNA · 2025Article
- Integrative functional genomics reveals transcriptional regulatory function of risk alleles for metabolic liver disease.Research square · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Sexually Dimorphic Effects of CYP2B6 in the Development of Fasting-Mediated Steatosis in Mice: Role of the Oxylipin Products 9-HODE and 9-HOTrE.Biomedicines · 2025Article
- Steatotic liver disease and cancer: from pathogenesis to therapeutic targets.eGastroenterology · 2025Review
- Advances in intrahepatic and extrahepatic vascular dysregulations in cirrhotic portal hypertension.Frontiers in medicine · 2025Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Liver injury stimulates hepatocyte replication and hepatic stellate cell (HSC) activation, thereby driving liver regeneration. Aberrant HSC activation induces liver fibrosis. However, mechanisms underlying liver regeneration and fibrosis remain poorly understood. Here, we identify hepatic Snai1 and Snai2 as important transcriptional regulators for liver regeneration and fibrosis. Partial hepatectomy or CCl4 treatment increases occupancies of Snai1 and Snai2 on cyclin A2 and D1 promoters in the liver. Snai1 and Snai2 in turn increase promoter H3K27 acetylation and cyclin A2/D1 expressions. Hepatocyte-specific deletion of both Snai1 and Snai2, but not one alone, suppresses liver cyclin A2/D1 expression and regenerative hepatocyte proliferation after hepatectomy or CCl4 treatments but augments CCl4-stimulated HSC activation and liver fibrosis. Conversely, Snai2 overexpression in the liver enhances hepatocyte replication and suppresses liver fibrosis after CCl4 treatment. These results suggest that hepatic Snai1 and Snai2 directly promote, via histone modifications, reparative hepatocyte replication and indirectly inhibit liver fibrosis.
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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.