Transforming Growth Factor Beta Signaling in Wound Healing
Summary
Transforming growth factor beta (TGF-β) encompasses a family of three related cytokines that orchestrate the cellular and molecular events of wound repair. Upon injury, TGF-β is released from platelets and activated in the extracellular matrix to regulate inflammation, cell proliferation, migration and extracellular matrix deposition. Canonical signalling proceeds via TGF-β type I and II receptor serine/threonine kinases and Smad transcription factors, while non-canonical cascades engage pathways such as PI3K/AKT, MAPK and Rho GTPases. These coordinated signals direct keratinocyte re-epithelialisation, fibroblast-to-myofibroblast transition, angiogenesis and immune cell behaviour, ensuring timely closure and tissue remodelling. Isoform-specific actions of TGF-β1, TGF-β2 and TGF-β3 influence the balance between scar formation and regenerative healing. Dysregulation of TGF-β signalling underlies chronic wounds, excessive fibrosis and impaired tissue function. Advances in delivery modalities, receptor modulation and targeted inhibitors are now translating mechanistic insights into therapeutic strategies for improved healing outcomes.
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Transforming Growth Factor Beta Signaling in Wound Healing publication trend
The graph below shows the total number of articles in transforming growth factor beta signaling in wound healing across all publications each year (not limited to Nature Index journals).
Technical terms
TGF-β: A family of multifunctional cytokines that regulate inflammation, cell proliferation, differentiation and extracellular matrix synthesis during wound healing.
Smad proteins: Intracellular effectors of canonical TGF-β signalling that translocate to the nucleus to regulate gene transcription.
BAMBI: A pseudoreceptor structurally related to TGF-β type I receptors that inhibits Smad-dependent signalling.
Ferroptosis: An iron-dependent form of regulated cell death driven by lipid peroxidation.
Conditioned medium: Culture fluid containing secreted bioactive molecules from donor cells used to influence recipient cell behaviour.
PI3K/AKT pathway: A non-canonical signalling cascade promoting cell survival, proliferation and migration downstream of growth factors and cytokines.
References
- TGF-β signaling in health, disease and therapeutics. Signal Transduction and Targeted Therapy (2024).
- Signalling by Transforming Growth Factor Beta Isoforms in Wound Healing and Tissue Regeneration. Journal of Developmental Biology (2016).
- δ-Tocotrienol preconditioning improves the capability of bone marrow-derived mesenchymal stem cells in promoting wound healing by inhibiting BACH1-related ferroptosis. Cell Death Discovery (2023).
- Increased Levels of BAMBI Inhibit Canonical TGF-β Signaling in Chronic Wound Tissues. Cells (2023).
- Effects of an Adipose Mesenchymal Stem Cell-Derived Conditioned medium and TGF-β1 on Human Keratinocytes In Vitro. International Journal of Molecular Sciences (2023).
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