ArticleJHEP reports : innovation in hepatology2025
Myeloid TGF-β signaling shapes liver macrophage heterogeneity and metabolic liver disease pathogenesis.
Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Myeloid MMP14 couples extracellular proteolysis to inflammatory and metabolic remodeling during obesity.Cell reports · 2026Article
- Integrated transcriptomic analysis identifies liver aging-driven fibrosis signatures and reveals therapeutic strategies based on medicine-food homology.NPJ science of food · 2026Article
- Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.Frontiers in cell and developmental biology · 2026Article
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Macrophages: friend or foe in diabetes pathogenesis and therapy.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Background & Aims: Cellular heterogeneity of innate immune cells, such as macrophages, in the liver is a hallmark of metabolic dysfunction-associated steatohepatitis (MASH) pathogenesis. However, the mechanisms shaping liver macrophage heterogeneity and function during disease progression remain poorly understood. Methods: Control or myeloid-specific Results: We identified TGF-β signaling as a crucial regulator of disease-associated expansion of Trem2 Conclusions: These findings identify myeloid TGF-β signaling as a key driver of liver macrophage heterogeneity and polarization within the microenvironment during the progression of MASH and MASH-associated liver cancer. Impact and implications: Our study reveals that myeloid TGF-β signaling plays a crucial role in shaping liver macrophage heterogeneity, which in turn influences the pathogenesis of metabolic liver disease. These findings are particularly important for researchers studying immune-metabolic interactions and for clinicians seeking new therapeutic strategies for liver disorders. By elucidating how TGF-β signaling regulates macrophage function, our work paves the way for targeted interventions that modulate immune responses to improve liver health. Future research should consider the potential translational applications of these findings while addressing limitations related to model systems and human variability.
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Registered trials
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