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Updated: Mar 30, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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[OMT inhibited TGF-β1-induced cardiac fibroblast proliferation via down-regulating p38MAPK phosphorylation in vitro]

Hai Xiao, Yi-ni Xu, Hong Luo

    Zhongguo Zhong Yao Za Zhi = Zhongguo Zhongyao Zazhi = China Journal of Chinese Materia Medica
    |November 11, 2015
    PubMed
    Abstract

    Insights

    OMT significantly inhibits fibroblast proliferation and collagen deposition induced by TGF-β1. This effect is mediated by inhibiting p38MAPK phosphorylation, offering potential therapeutic insights.

    Area of Science:

    • Cell Biology
    • Pharmacology
    • Biochemistry

    Background:

    • Fibroblast proliferation and extracellular matrix deposition are key in fibrotic diseases.
    • Transforming growth factor-beta 1 (TGF-β1) is a critical mediator of these processes.
    • Investigating novel inhibitors of TGF-β1 signaling is crucial for therapeutic development.

    Purpose of the Study:

    • To evaluate the inhibitory effects of OMT on TGF-β1-induced fibroblast proliferation.
    • To elucidate the underlying molecular mechanism of OMT's action.

    Main Methods:

    • Cell proliferation was assessed using MTT assays.
    • Immunocytochemistry identified vimentin and α-SMA.
    • Collagen deposition was quantified via Sirius red staining and Western blotting.
    • Western blotting analyzed the phosphorylation status of p38MAPK.

    Main Results:

    • OMT significantly inhibited TGF-β1-induced fibroblast proliferation (P < 0.01).
    • OMT reduced collagen type I and III deposition.
    • OMT attenuated TGF-β1-induced p38MAPK phosphorylation.

    Conclusions:

    • OMT effectively inhibits fibroblast proliferation and collagen deposition stimulated by TGF-β1.
    • The mechanism involves the inhibition of p38MAPK phosphorylation.
    • OMT demonstrates potential as a therapeutic agent for fibrotic conditions.

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