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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Updated: Jun 22, 2026

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

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Published on: September 14, 2021

Transforming growth factor-beta in systemic sclerosis (scleroderma).

John Varga¹, Michael L Whitfield

¹Feinberg School of Medicine, Northwestern University, Chicago IL, USA. varga@northwestern.edu

Frontiers in Bioscience (Scholar Edition)

|June 2, 2009

Summary

This summary is machine-generated.

Transforming growth factor-beta (TGF-beta) drives systemic sclerosis (SSc) pathogenesis. Understanding TGF-beta

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Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

Area of Science:

Immunology
Rheumatology
Molecular Biology

Background:

Systemic sclerosis (SSc) is a chronic connective tissue disease marked by fibrosis.
Deregulated transforming growth factor-beta (TGF-beta) signaling is central to SSc pathogenesis.
SSc exhibits heterogeneous clinical manifestations and molecular subtypes.

Purpose of the Study:

To investigate the role of TGF-beta in regulating fibroblast function in SSc.
To explore potential targeted therapies for SSc based on TGF-beta pathways.
To understand the molecular signatures underlying SSc heterogeneity.

Main Methods:

Transcriptional profiling of gene expression in SSc target organs.
Analysis of TGF-beta signaling pathways in fibroblasts.
Investigating fibroblast function in the context of SSc.

Main Results:

TGF-beta activity and responses are key contributors to SSc.
Fibroblast function is significantly regulated by TGF-beta.
Distinct molecular signatures define SSc subgroups.

Conclusions:

Targeted therapies blocking TGF-beta signaling are promising for SSc treatment.
Further research into TGF-beta's role in SSc may yield novel anti-fibrotic strategies.
Understanding molecular subtypes is crucial for personalized SSc treatment.