ArticleScience advances2024
Atf3-mediated metabolic reprogramming in hepatic macrophage orchestrates metabolic dysfunction-associated steatohepatitis.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- The role of protein palmitoylation in disease pathogenesis and therapeutic innovation.Annals of medicine · 2026Review
- Obstructive sleep apnea mediates the association between body mass index and metabolic dysfunction-associated steatotic liver disease in patients with obesity.Hepatology international · 2026Article
- ZDHHC17-mediated IKKβ palmitoylation suppresses NF-κB signaling to mitigate the progression of liver fibrosis.iScience · 2026Article
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- ATF3 Modulates the Endoplasmic Reticulum Stress-Induced Impairment of Milk Synthesis in Bovine Mammary Epithelial Cells.International journal of molecular sciences · 2026Article
- Trem1 regulates neutrophil metabolism and recruitment in lung ischemia-reperfusion injury.Redox biology · 2026Article
- Palmitoylation-dependent regulation of innate and adaptive immunity: molecular insights and translational opportunities.Cellular & molecular biology letters · 2026Review
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
- The Transcription Factor DDIT3 Regulates Macrophage Function by Inhibiting KLF10 to Attenuate ALI/ARDS Inflammation.Inflammation · 2026Article
- Advances in the application of insulin resistance-related indicators in the clinical evaluation of metabolic dysfunction-associated steatotic liver disease.Frontiers in gastroenterology (Lausanne, Switzerland) · 2026Review
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- Reactive sulfur species as emerging immunomodulators: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
- The dual role of ATF3 in myocardial repair through macrophage regulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Hepatic activating transcription factor 3 protects against systemic inflammation by attenuating lipotoxicity.Metabolism open · 2025Article
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Metabolism-driven posttranslational modifications and immune regulation: Emerging targets for immunotherapy.Science advances · 2025Review
- Polynucleotides Enhance Collagen Synthesis via Modulating Phosphoenolpyruvate Carboxykinase 1 in Senescent Macrophages: Experimental Evidence.International journal of molecular sciences · 2025Article
- Recent advances in S-palmitoylation and its emerging roles in human diseases.Journal of hematology & oncology · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is regulated by complex interplay between the macrophages and surrounding cells in the liver. Here, we show that Atf3 regulates glucose-fatty acid cycle in macrophages attenuates hepatocyte steatosis, and fibrogenesis in hepatic stellate cells (HSCs). Overexpression of Atf3 in macrophages protects against the development of MASH in Western diet-fed mice, whereas Atf3 ablation has the opposite effect. Mechanistically, Atf3 improves the reduction of fatty acid oxidation induced by glucose via forkhead box O1 (FoxO1) and Cd36. Atf3 inhibits FoxO1 activity via blocking Hdac1-mediated FoxO1 deacetylation at K242, K245, and K262 and increases Zdhhc4/5-mediated CD36 palmitoylation at C3, C7, C464, and C466; furthermore, macrophage Atf3 decreases hepatocytes lipogenesis and HSCs activation via retinol binding protein 4 (Rbp4). Anti-Rbp4 can prevent MASH progression that is induced by Atf3 deficiency in macrophages. This study identifies Atf3 as a regulator of glucose-fatty acid cycle. Targeting macrophage Atf3 or Rbp4 may be a plausible therapeutic strategy for MASH.
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