ArticleJournal of Zhejiang University. Science. B2023
Vitamin D receptor (VDR) mediates the quiescence of activated hepatic stellate cells (aHSCs) by regulating M2 macrophage exosomal smooth muscle cell-associated protein 5 (SMAP-5).
Article in Journal of Zhejiang University. Science. B, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- The impact of obesity on bone health: molecular pathways, metabolic interactions, and associated pathologies.International journal of obesity (2005) · 2026Review
- Senkyunolide I suppresses hepatic stellate cell activation and liver fibrosis by reprogramming VDR-dependent fatty acid metabolism.Chinese medicine · 2025Article
- Bile acids and their receptors in hepatic immunity.Liver research (Beijing, China) · 2025Review
- Extracellular Vesicles in Viral Liver Diseases.Viruses · 2024Review
- Tackling exosome and nuclear receptor interaction: an emerging paradigm in the treatment of chronic diseases.Military Medical Research · 2024Review
- Role of Exosomal Modulation of Macrophages in Liver Fibrosis.Journal of clinical and translational hepatology · 2024Review
- Non-Alcoholic Fatty Liver Disease and Bone Tissue Metabolism: Current Findings and Future Perspectives.International journal of molecular sciences · 2023Review
- The regulatory role and mechanism of exosomes in hepatic fibrosis.Frontiers in pharmacology · 2023Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
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Abstract
An effective therapeutic regimen for hepatic fibrosis requires a deep understanding of the pathogenesis mechanism. Hepatic fibrosis is characterized by activated hepatic stellate cells (aHSCs) with an excessive production of extracellular matrix. Although promoted activation of HSCs by M2 macrophages has been demonstrated, the molecular mechanism involved remains ambiguous. Herein, we propose that the vitamin D receptor (VDR) involved in macrophage polarization may regulate the communication between macrophages and HSCs by changing the functions of exosomes. We confirm that activating the VDR can inhibit the effect of M2 macrophages on HSC activation. The exosomes derived from M2 macrophages can promote HSC activation, while stimulating VDR alters the protein profiles and reverses their roles in M2 macrophage exosomes. Smooth muscle cell-associated protein 5 (SMAP-5) was found to be the key effector protein in promoting HSC activation by regulating autophagy flux. Building on these results, we show that a combined treatment of a VDR agonist and a macrophage-targeted exosomal secretion inhibitor achieves an excellent anti-hepatic fibrosis effect. In this study, we aim to elucidate the association between VDR and macrophages in HSC activation. The results contribute to our understanding of the pathogenesis mechanism of hepatic fibrosis, and provide potential therapeutic targets for its treatment.
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