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Updated: Aug 23, 2026

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay
Published on: September 14, 2021
TGF-beta-induced SMAD signaling and gene regulation: consequences for extracellular matrix remodeling and wound
Meinhard Schiller1, Delphine Javelaud, Alain Mauviel
1INSERM U532, Institut de Recherche sur la Peau, Université Paris VII, Hôpital Saint-Louis, 1 Avenue Claude Vellefaux, 75010 Paris, France.
Abstract:
Members of the transforming growth factor-beta (TGF-beta) superfamily are pleiotropic cytokines that have the ability to regulate numerous cell functions, including proliferation, differentiation, apoptosis, epithelial-mesenchymal transition, and production of extracellular matrix, allowing them to play an important role during embryonic development and for maintenance of tissue homeostasis. Three TGF-beta isoforms have been identified in mammals. They propagate their signal via a signal transduction network involving receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins. Upon phosphorylation and oligomerization, the latter move into the nucleus to regulate transcription of target genes. This review will summarize recent advances in the understanding of the mechanisms underlying SMAD modulation of extracellular matrix gene expression in the context of wound healing and tissue fibrosis.
Insights
Transforming growth factor-beta (TGF-beta) superfamily cytokines regulate cell functions. This review details SMAD protein mechanisms in extracellular matrix gene expression during wound healing and fibrosis.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Transforming growth factor-beta (TGF-beta) superfamily cytokines are crucial for embryonic development and tissue homeostasis.
- These cytokines regulate key cellular processes like proliferation, differentiation, apoptosis, and epithelial-mesenchymal transition.
- Three mammalian TGF-beta isoforms exist, signaling through receptor kinases and SMAD proteins.
Purpose of the Study:
- To summarize recent advances in understanding SMAD protein modulation of extracellular matrix (ECM) gene expression.
- To explore the role of TGF-beta signaling in wound healing and tissue fibrosis.
Main Methods:
- Review of recent scientific literature on TGF-beta signaling pathways.
- Analysis of SMAD protein interactions and transcriptional regulation.
- Focus on ECM gene expression mechanisms.
Main Results:
- SMAD proteins, upon phosphorylation and oligomerization, translocate to the nucleus.
- SMAD proteins regulate the transcription of target genes, including those involved in ECM production.
- Recent advances shed light on specific mechanisms of SMAD-mediated ECM regulation.
Conclusions:
- TGF-beta signaling, mediated by SMAD proteins, is a critical regulator of ECM gene expression.
- Understanding these mechanisms is vital for addressing pathological conditions like fibrosis and improving wound healing.
- Further research into SMAD modulation pathways holds therapeutic potential.
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