ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
LIMA1 O-GlcNAcylation Promotes Hepatic Lipid Deposition through Inducing β-catenin-Regulated FASn Expression in Metabolic Dysfunction-Associated Steatotic Liver Disease.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- TRAIP Mediates Alcohol-Induced Liver Injury through Regulating β-catenin Ubiquitin Degradation via Direct Interaction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Emerging roles of O-GlcNAcylation in tumorigenesis, immunosuppression and drug resistance (Review).Oncology letters · 2026Review
- Glycosylation modification: a trigger for obesity and its complications?Molecular medicine (Cambridge, Mass.) · 2026Review
- GALNT7 promotes the malignant progression of gastrointestinal stromal tumors by regulating KIT O-GalNAc glycosylation.Precision clinical medicine · 2026Article
- Extracellular Vesicles: Orchestrators of Intrahepatic and Systemic Crosstalk in Metabolic Dysfunction-Associated Steatotic Liver Disease.Pharmaceutics · 2026Review
- Inhibition of Breast Cancer Bone Metastasis by LRP5-Overexpressing Osteocytes via the LIMA1/MYO5B Signaling Axis.International journal of molecular sciences · 2026Article
- Article
- Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation.International journal of biological sciences · 2026Article
- LIMA1 O-GlcNAcylation Promotes Hepatic Lipid Deposition through Inducing β-catenin-Regulated FASn Expression in Metabolic Dysfunction-Associated Steatotic Liver Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Hepatic lipid deposition is a key factor in progressing metabolic dysfunction-associated steatotic liver disease (MASLD). This study investigates the impact of the LIM domain and actin-binding protein 1 (LIMA1) on hepatic steatotic in MASLD and explore the underlying mechanisms. Increased levels of LIMA1 is observed in both serum and serum sEV of metabolic dysfunction-associated steatohepatitis (MASH) patients compared to healthy controls, with AUROC values of 0.76 and 0.86, respectively. Furthermore, increased LIMA1 O-GlcNAcylation is observed in mouse models of MASLD, and steatotic hepatocytes. Mechanistic studies revealed that steatosis upregulated Host cell factor 1 (HCF1) and O-GlcNAc transferase (OGT) expression, leading to catalyzed O-GlcNAcylation at the T662 site of LIMA1 and subsequent inhibition of its ubiquitin-dependent degradation. O-GlcNAcylation of LIMA1 enhances hepatocyte lipid deposition by activating β-catenin/FASn-associated signaling. Additionally, compared with their AAV8-TBG-LIMA1-WT counterparts, AAV8-TBG-LIMA1
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