ArticleNature communications2025
Trajectory analysis of hepatic stellate cell differentiation reveals metabolic regulation of cell commitment and fibrosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Article
- Article
- Association between changes in HBsAb levels and hepatic adverse events after HBsAg clearance in non-cirrhotic chronic hepatitis B patients.BMC infectious diseases · 2026Observational
- Fibroblast growth factor 10 attenuates advanced liver fibrosis through hepatocyte fibroblast growth factor receptor 2 signalling.Clinical and translational medicine · 2026Article
- Residual bile flow shapes PPARγ-mediated antifibrotic responses in experimental segmental cholestasis.Scientific reports · 2026Article
- The Hepatic Transcriptomes of Two Mouse Models of Liver Fibrosis Reveal Shared Molecular Patterns Associated with a Common Dysregulation of Folate Metabolism.The Journal of nutrition · 2026Article
- Molecular mechanisms mediated by liquid-liquid phase separation in chronic liver disease progression.iScience · 2025Review
- Liver developmental microenvironment promotes iHSC generation from human iPSCs.Scientific reports · 2025Article
- Immunometabolic integration in therapeutic strategies for managing MASLD.Frontiers in pharmacology · 2025Review
- Challenges ofFrontiers in cell and developmental biology · 2025Review
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Authors and funding
41 authors.
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Abstract
Defining the trajectory of cells during differentiation and disease is key for uncovering the mechanisms driving cell fate and identity. However, trajectories of human cells remain largely unexplored due to the challenges of studying them with human samples. In this study, we investigate the proteome trajectory of iPSCs differentiation to hepatic stellate cells (diHSCs) and identify RORA as a key transcription factor governing the metabolic reprogramming of HSCs necessary for diHSCs' commitment, identity, and activation. Using RORA deficient iPSCs and pharmacologic interventions, we show that RORA is required for early differentiation and prevents diHSCs activation by reducing the high energetic state of the cells. While RORA knockout mice have enhanced fibrosis, RORA agonists rescue multi-organ fibrosis in in vivo models. Notably, RORA expression correlates negatively with liver fibrosis and HSCs activation markers in patients with liver disease. This study reveals that RORA regulates cell metabolic plasticity, important for mesoderm differentiation, pericyte quiescence, and fibrosis, influencing cell commitment and disease.
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