ArticleScience translational medicine2023
Hepatocytes demarcated by EphB2 contribute to the progression of nonalcoholic steatohepatitis.
Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 65 citations in OpenAlex.
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- TGFβ activity stabilizes ACC1 to increase de novo lipogenesis in metabolic liver disease.Molecular metabolism · 2026Article
- Fatty acid-activated proton transporter SR4 prevents hepatic steatosis and metabolic alterations in diabetic mice by improving mitochondria function, energy balance and oxidative stress.Experimental and therapeutic medicine · 2026Article
- Integrative analyses elucidate transcriptional regulatory functions of risk alleles for metabolic liver disease.Nature genetics · 2026Article
- Reduction in Hepatic Phosphatidylcholine Biosynthesis Promotes MASH Through Copper Deficiency.bioRxiv : the preprint server for biology · 2026Article
- The role of hepatocyte epigenetics in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Communications medicine · 2026Review
- The Metabolite Differences in Vascular Smooth Muscle Cells of Abdominal Aortic Aneurysm Revealed by Untargeted Metabolomics.Biomedicines · 2026Article
- Lianhe Xiaozhi ointment ameliorates metabolic dysfunction-associated steatotic liver diseaseWorld journal of gastroenterology · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Scar-associated endothelial-stellate cellular crosstalk drives fibrosis resolution in MASH.Cell reports · 2026Article
- ATF3 and HNF4A: an oxidative phosphorylation and cholesterol homeostasis-associated diagnostic and therapeutic repurposing framework target for metabolic dysfunction-associated steatohepatitis patients.Frontiers in medicine · 2026Article
- Notch signaling in liver diseases: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Advanced multifunctional nano-delivery platform focusing on treating diseases related to lipid metabolism via targeted intervention in various lipid metabolic processes.Military Medical Research · 2025Review
- Pathogenesis of metabolic dysfunction-associated steatotic liver disease and donor liver damage.iLIVER · 2025Review
- AAV capsid prioritization in normal and steatotic human livers maintained by machine perfusion.Nature biotechnology · 2025Article
- Spatially resolved multi-omics of human metabolic dysfunction-associated steatotic liver disease.Nature genetics · 2025Article
- Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025Review
- Integrative functional genomics reveals transcriptional regulatory function of risk alleles for metabolic liver disease.Research square · 2025Article
- Sodium nitrate protects against metabolic syndrome by sialin-mediated macrophage rebalance.Signal transduction and targeted therapy · 2025Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Current therapeutic strategies for treating nonalcoholic steatohepatitis (NASH) have failed to alleviate liver fibrosis, which is a devastating feature leading to hepatic dysfunction. Here, we integrated single-nucleus transcriptomics and epigenomics to characterize all major liver cell types during NASH development in mice and humans. The bifurcation of hepatocyte trajectory with NASH progression was conserved between mice and humans. At the nonalcoholic fatty liver (NAFL) stage, hepatocytes exhibited metabolic adaptation, whereas at the NASH stage, a subset of hepatocytes was enriched for the signatures of cell adhesion and migration, which were mainly demarcated by receptor tyrosine kinase ephrin type B receptor 2 (EphB2). EphB2, acting as a downstream effector of Notch signaling in hepatocytes, was sufficient to induce cell-autonomous inflammation. Knockdown of Ephb2 in hepatocytes ameliorated inflammation and fibrosis in a mouse model of NASH. Thus, EphB2-expressing hepatocytes contribute to NASH progression and may serve as a potential therapeutic target.
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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.