ArticleMolecular biology reports2026
Antifibrotic activity of Schistosoma japonicum-derived sja-miR-2a-3p in carbon tetrachloride-induced liver fibrosis.
Article in Molecular biology reports, 2026. 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 consequence of chronic liver injury and is driven largely by persistent activation of hepatic stellate cells and excessive extracellular matrix deposition. We previously identified Schistosoma japonicum-derived sja-miR-2a-3p as a parasite-derived microRNA with antifibrotic activity in schistosomiasis-associated liver fibrosis. Whether this cross-species regulatory molecule also modulates fibrogenesis beyond the context of schistosome infection remains unclear. METHODS AND
resultsWe investigated the effects of sja-miR-2a-3p in a carbon tetrachloride-induced mouse model of liver fibrosis. Mice received systemic administration of sja-miR-2a-3p agomir during CCL₄-induced fibrogenesis, followed by assessment of histological liver injury, fibrosis, inflammation, HSC activation, HSC-associated apoptotic activity, and transcriptomic alterations. sja-miR-2a-3p agomir administration increased sja-miR-2a-3p abundance in serum and liver tissues and markedly attenuated CCL₄-induced hepatic injury and fibrosis, as evidenced by reduced liver weight index, Ishak fibrosis scores, collagen deposition, and hepatic hydroxyproline content. sja-miR-2a-3p treatment also suppressed HSC activation and extracellular matrix production, with decreased expression of α-SMA, Col1α1, Col3α1, and TGF-β. Moreover, enhanced cleaved caspase-3 signals were observed in desmin-positive HSCs, consistent with increased apoptotic activity in activated HSCs. Hepatic expression of the inflammatory mediators TNF-α, IL-1β, and IL-6 was also reduced. Whole-liver transcriptomic analysis further showed treatment-associated downregulation of extracellular matrix-, cytokine-, chemokine-, NF-κB-, IL-17-, and TNF-related pathways.
conclusionssja-miR-2a-3p attenuates CCL₄-induced liver fibrosis in mice, accompanied by reduced HSC activation and extracellular matrix accumulation, enhanced HSC-associated apoptotic activity, and attenuation of inflammatory signaling. These findings extend the biological activity of sja-miR-2a-3p from schistosomiasis-associated fibrosis to a chemically induced fibrosis model and support further investigation of helminth-derived regulatory miRNAs as modulators of host fibrotic responses.
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