ArticleHepatology (Baltimore, Md.)2025
Metabolic reprogramming of immune cells in MASH.
Article in Hepatology (Baltimore, Md.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed.
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- Metabolic Dysfunction-Associated Steatohepatitis: Is There Evidence for Fractured CD4+ T-Cell Tolerance in the Immunopathogenesis.Cellular and molecular gastroenterology and hepatology · 2026Review
- When the Liver Flares: Inflammatory and Immunometabolic Mechanisms Driving the Transition from MASLD to MASH.Inflammation · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- F13A1-Mediated Macrophage Activation Promotes MASH Progression via the PKM2/HIF1A Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The immunometabolic nature of MASH: framing immune cells within metabolic dysfunction.Frontiers in immunology · 2026Review
- Metabolic dysfunction and GZMKFrontiers in immunology · 2026Review
- Integrating single-cell RNA-seq and machine learning to dissect polyamine metabolism in metabolic dysfunction-associated steatotic liver disease.Frontiers in medicine · 2026Article
- Targeting macrophage metabolism: mechanisms, cellular crosstalk and implications in obesity-associated metabolic diseases.Frontiers in immunology · 2026Review
- Hepatic immune microenvironment dynamics in severe obesity and post-bariatric surgery: insights from immunohistochemical analysis.Frontiers in immunology · 2026Article
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
- NAFLD-associated immune remodeling in colorectal cancer liver metastasis: mechanisms and implications for immunotherapy.Frontiers in immunology · 2026Review
- Primary Human Tissue Models for Metabolic Dysfunction-Associated Liver Disease - toward Streamlining Drug Discovery with Patient-Derived Assays.Advanced biology · 2025Review
- Roles of short-chain fatty acids in metabolic dysfunction-associated steatotic liver disease and metabolic dysfunction-associated steatohepatitis.World journal of hepatology · 2025Review
- Betulinic acid as a novel AT1R inhibitor: attenuation of liver fibrosis via modulation of endothelial-mesenchymal transition in chronic hepatic injury.Journal of translational medicine · 2025Article
- Multifaceted Interactions Between Bile Acids, Their Receptors, and MASH: From Molecular Mechanisms to Clinical Therapeutics.Molecules (Basel, Switzerland) · 2025Review
- Insulin Modulates NK Cell Activity in Liver Fibrosis MASH Patients via the STING Pathway.Cells · 2025Article
- Recent advances in non-alcoholic steatohepatitis-associated hepatocellular carcinoma: immune cells, metabolic dysregulation, and therapeutic strategies.Frontiers in oncology · 2025Review
- Immunometabolic integration in therapeutic strategies for managing MASLD.Frontiers in pharmacology · 2025Review
- Three Dimensional Biomimetic Liver Models to Reconstitute Metabolic Dysfunction-Associated Steatohepatitis (MASH)Journal of clinical and experimental hepatologyReview
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease, previously known as NAFLD, affects ~30% of adults worldwide. Approximately 1 out of 6 patients with metabolic dysfunction-associated steatotic liver disease progress to metabolic dysfunction-associated steatohepatitis (MASH) and potentially evolve toward cirrhosis and HCC. This condition imposes a significant burden on global health. Although MASH is primarily a metabolic disorder, immune cells play a crucial role in its development. The activation of immune cells involves alterations in transcription and protein synthesis, which require metabolic adaptation of cellular substrate metabolism, including glucose and lipid metabolism. Moreover, the lipid-rich environment of the liver can affect the metabolism of immune cells. In this review, we delineate the metabolic profiles of immune cells in MASH, focusing on macrophages and T cells, and discuss the impact of targeting cellular metabolism on these cells along with clinical trial outcomes. Macrophages in MASH are characterized by increased glycolysis, compromised oxidative phosphorylation, and augmented lipid uptake, synthesis, and fatty acid oxidation, all of which contribute to their inflammatory phenotype. Lymphocytes, such as T cells and NK cells, exhibit impaired metabolic functions that hamper their immune surveillance capabilities and facilitate the development of HCC. However, research on the metabolic characteristics of other types of immune cells remains limited. With the development of single-cell genomics and animal models of MASH, we anticipate that further studies in this compelling field may shed light on the pathogenesis of MASH and pave the way for novel therapeutic strategies.
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Registered trials
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