ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Asprosin-FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation through PPARα Contributing to MASLD Development.
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 15 papers.
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Who cites it
15 citing papers in PubMed.
- Flavonoids for MASLD: Hepatic Lipid Targets, Biopharmaceutic Barriers, and Formulation Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Cyanobacteria-derived near-infrared autofluorescent exosomes enabling synergistic brain lesion imaging and neuroprotection.Bioactive materials · 2026Article
- Thiamine modulates the mammary inflammation, antioxidant function and lactation performance in lactating sheep under heat-stress conditions.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Jiuwei Xiaozhi Decoction Alleviates High-Fat Diet-Induced MASLD by Suppressing Hepatic SREBP2-Driven Cholesterogenesis and Restoring PPARα-Mediated Fatty Acid Oxidation.Chemical biology & drug design · 2026Article
- Review
- Dehydrocostus lactone attenuates hepatic steatosis by regulating fatty acid oxidation and lipid metabolism: integrated transcriptomic and metabolomic analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Chronic Intermittent Hypoxia Exacerbates High-Fat Diet-Induced MASLD Through Lipid Metabolic Reprogramming, Impaired Antioxidant Defense, and NF-κB/NLRP3 Activation.Biomolecules · 2026Article
- Increased WNT10B/FOXO6 signaling promotes cell fate transition in renal tubular cells to aggravate renal inflammation and fibrosis.Nature communications · 2026Article
- Metabolic Myokines and Adipokines in the Follicular Microenvironment: Implications for Oocyte Competence and IVF Outcomes.International journal of molecular sciences · 2026Review
- Regulatory effects of hawthorn on lipid metabolic homeostasis: mechanisms, evidences, and perspectives.Frontiers in nutrition · 2026Review
- Transcriptomic analysis identifies FABP5 as a candidate regulator of lipid accumulation in metabolic dysfunction-associated fatty liver disease.Frontiers in endocrinology · 2026Article
- Targeting the FABP Axis: Interplay Between Lipid Metabolism, Neuroinflammation, and Neurodegeneration.Cells · 2025Review
- Macrophage and inflammation in diabetes and metabolic dysfunction-associated steatotic liver disease: From mechanisms to therapeutic strategies.World journal of diabetes · 2025Review
- Asprosin-FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation through PPARα Contributing to MASLD Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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14 authors.
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Abstract
Alterations in liver metabolism play a pivotal role in the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Asprosin is reported to be released from white adipose tissue during fasting and targets the liver. However, the role of asprosin, especially from organs other than adipose tissue, in MASLD remains poorly understood. These findings demonstrate that plasma asprosin levels are significantly elevated in MASLD patients and animal models. Additionally, asprosin expression increased in the liver of MASLD mice. Hepatocyte-specific overexpression of asprosin impairs mitochondrial fatty acid β-oxidation (FAO), whereas its knockdown not only enhances FAO in mice but also compensates for fenofibrate's limitations in MASLD treatment. Mechanistic investigations reveal that the interaction of asprosin with FABP5 facilitates its abnormal nuclear localization, and asprosin directly bound to and inhibites peroxisome proliferator-activated receptor elements (PPREs), which negatively regulated PPARα transcriptional activity, and disrupts hepatic FAO pathways. GalNAc-siRNAs targeting hepatic FABP5 ameliorate hepatic steatosis. These findings reveal that the secretory adipose factor asprosin is expected to act as a biological marker for early clinical diagnosis and prognostic evaluation of MASLD. Moreover, targeting hepatic asprosin gene inhibition and GalNAc-siRNAs to inhibit hepatic FABP5 both offer potential therapeutic benefits in the treatment of MASLD.
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