ArticleJournal of molecular histology2026
Yohimbine attenuates bleomycin-induced skin fibrosis by modulating the PI3K/Akt-MAPK signaling: an integrated network pharmacology and in vivo study.
Article in Journal of molecular histology, 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
Skin fibrosis is a chronic inflammatory disorder characterized by excessive extracellular matrix (ECM) deposition and aberrant fibroblast activation, leading to tissue stiffening and progressive functional impairment. Despite its clinical prevalence, no FDA-approved therapies are currently available, highlighting a significant unmet medical need. The present study investigated the anti-fibrotic potential of yohimbine using an integrated network pharmacology approach and a bleomycin (BLM)-induced murine skin fibrosis model. Network pharmacology identified 168 overlapping targets between yohimbine and skin fibrosis, while KEGG enrichment highlighted the PI3K/Akt and MAPK pathways as key antifibrotic signaling mechanisms. Subcutaneous administration of BLM (3 mg/kg) for 28 days induced marked skin fibrosis compared with sham control. Yohimbine treatment at 2.5 and 5 mg/kg attenuated bleomycin (BLM)-induced skin fibrosis, with the 5 mg/kg dose demonstrating a more consistent antifibrotic response compared with the BLM group. Molecular analyses demonstrated that yohimbine suppressed the pro-fibrotic (Ccn2, α-Sma, Vimentin, Zeb, and Snail) and inflammatory markers (Tnf-α) expression. Furthermore, yohimbine restored the expression of antifibrotic (Hgf) and antioxidant (Gstp1, Nrf2, and Hmox1) markers, while reducing ECM-associated markers, including Fibronectin (FN1) and Collagen Type III (COL3α1), at both mRNA and protein levels. Histopathological, Masson's trichrome, and Sirius red/fast green collagen staining analysis further demonstrated that yohimbine treatment significantly (p < 0.05) reduced collagen deposition and restored normal skin architecture. Collectively, these findings demonstrate that yohimbine attenuates skin fibrosis by suppressing inflammatory and fibrotic responses, potentially through modulation of PI3K/Akt-MAPK signaling, and may represent a potential lead for further investigation in fibrotic skin disorders.
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