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Updated: May 15, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

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Published on: October 27, 2020

[The role of TGF-beta activation on different pathological phenotypes in chronic rhinosinusitis]

Jinyin Xiang, Ji Shen, Suling Hong

    Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi = Journal of Clinical Otorhinolaryngology Head and Neck Surgery
    |January 1, 2013
    PubMed

    Insights

    Transforming growth factor-beta (TGF-beta) is key in chronic rhinosinusitis (CRS) subtypes. Dysregulation of TGF-beta activation contributes to CRS pathogenesis and different disease phenotypes.

    Area of Science:

    • Immunology
    • Molecular Biology
    • Pathogenesis Research

    Context:

    • Chronic rhinosinusitis (CRS) involves complex immune dysregulation.
    • Transforming growth factor-beta (TGF-beta) plays a central role in various CRS subtypes.
    • Understanding TGF-beta regulation is crucial for deciphering CRS pathogenesis.

    Purpose:

    • To review advancements in TGF-beta activation research.
    • To elucidate the role of TGF-beta in CRS pathogenesis.
    • To provide insights into human CRS investigation.

    Summary:

    • TGF-beta, a critical regulator, exists in latent forms suppressed by factors like LAP, LTBP, and fibrillin.
    • Activation of TGF-beta involves factors including integrins, proteases, and thrombospondin-1.
    • Dysregulation of TGF-beta activation is linked to fibrotic lung diseases and COPD, suggesting its role in CRS phenotypes.

    Impact:

    • Highlights the imbalance of TGF-beta regulating factors as a cause for CRS phenotypes.
    • Offers a deeper understanding of TGF-beta's role in CRS.
    • Informs future research directions for human CRS investigation.

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