ArticleAnimal cells and systems2021
Mirodenafil ameliorates skin fibrosis in bleomycin-induced mouse model of systemic sclerosis.
Article in Animal cells and systems, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Development of Local Bleomycin-Induced Hindlimb Model Recapitulating Skin Fibrosis and Vasculopathy of Systemic Sclerosis.Archives of plastic surgery · 2026Article
- Network pharmacology and in vivo experimental analysis for validating the antifibrotic potential of Punica granatum leaves against skin scleroderma: the role of oxidative stress, inflammation and TGF-β1/Snail 1/p-Smad 3 signaling pathway.Inflammopharmacology · 2026Article
- Article
- Ginsenoside Rg3 attenuates pulmonary fibrosis by inhibiting endothelial to mesenchymal transition.Animal cells and systems · 2023Article
- FAT10 Induces cancer cell migration by stabilizing phosphorylated ABI3/NESH.Animal cells and systems · 2023Article
- Hub genes, diagnostic model, and predicted drugs in systemic sclerosis by integrated bioinformatics analysis.Frontiers in genetics · 2023Article
- Chemical fluorescence-based dye staining for 3-dimensional histopathology analysis.Animal cells and systems · 2022Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by fibrosis of the skin and internal organs. Despite the recent advances in the pathogenesis and treatment of SSc, effective therapies for fibrosis caused by SSc have not yet been established. In this study, we investigated the potential role of mirodenafil, a potent phosphodiesterase 5 (PDE5) inhibitor, in the treatment of fibrosis in SSc. We used a bleomycin (BLM)-induced SSc mouse model to mimic the typical features of fibrosis in human SSc and examined the dermal thickness to assess the degree of skin fibrosis after staining with hematoxylin and eosin or Masson's trichrome stains. The effect of mirodenafil on the expression of profibrotic genes was also analyzed by treating fibroblasts with transforming growth factor (TGF)-β and mirodenafil. We showed that mirodenafil ameliorated dermal fibrosis and downregulated the protein levels of fibrosis markers including COL1A1 and α-SMA in the BLM-induced SSc mouse model. Further, using mouse embryonic fibroblasts and human lung fibroblasts, we demonstrated that the expression of collagen and profibrotic genes was reduced by treatment with mirodenafil. Finally, we showed that mirodenafil inhibited TGF-β-induced phosphorylation of Smad2/3 in fibroblasts, which suggested that this drug may ameliorate fibrosis by suppressing the TGF-β/Smad signaling pathway. Our findings suggest that mirodenafil possesses a therapeutic potential for treating fibrosis in SSc.
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