ArticleBMC medical genomics2025
Bone marrow mesenchymal stem cell-derived exosomes attenuate hepatic stellate cell activation through miR-223-3p-mediated mitophagy.
Article in BMC medical genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLiver fibrosis is a common pathological process in chronic liver diseases and effective treatments are lacking. The activation of hepatic stellate cells (HSCs) is a critical step in the development of liver fibrosis. Our previous research confirmed that bone marrow mesenchymal stem cell-derived exosomes (BMSC-exosomes) could regulate the level of miR-223-3p to alleviate intrahepatic inflammation, but whether they contribute to the protection of the liver against fibrosis remains unknown.
methodsIn this study, the antifibrotic function of BMSC-exosomes was validated through cell experiments. JS-1 cells (murine HSC line) were used as activated cells to simulate liver fibrosis. TGF-β is a stimulating factor for JS-1 cell activation. BMSC-exosomes were isolated via ultracentrifugation.
resultsOur results demonstrated that BMSC-exosomes internalized by JS-1 cells attenuated TGF-β-induced HSC activation and promoted HSC apoptosis. Moreover, BMSC-exosomes significantly reversed the upregulation of miR-223-3p levels and mitophagy induced by TGF-β. Luciferase activity reporter analysis further verified that hydroxy-3-methylglutaryl-CoA synthase 1 (HMGCS1) was a downstream target of miR-223-3p. By transfecting a miR-223-3p inhibitor, we found that downregulating miR-223-3p could increase the expression level of HMGCS1 and alleviate mitophagy, thereby reducing TGF-β-induced HSC activation and promoting HSC apoptosis.
conclusionsThese results suggest that BMSC-exosomes may have antifibrotic effects. The mechanism may be related to regulating miR-223-3p in HSCs to target HMGCS1 and mitophagy.
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