Synopsis

Source of validity: Scientific
Rating (out of 5): 3

Transforming growth factor-beta (TGF-β) is a cytokine with a well-characterized role in the regulation of wound healing and scar formation. Scientific studies, both in vitro and in vivo, have demonstrated that TGF-β is a central mediator in the formation of scar tissue. It stimulates fibroblast proliferation, collagen synthesis, and extracellular matrix deposition, all of which are key processes in tissue repair and fibrosis. Elevated levels of TGF-β are consistently observed in hypertrophic scars and keloids, suggesting its overactivity is associated with excessive scar tissue formation. Because of its pivotal role, TGF-β has been targeted therapeutically to modulate scarring. Experimental treatments, such as TGF-β inhibitors (e.g., neutralizing antibodies, soluble receptors, or antisense oligonucleotides), have shown promise in animal models and early human trials by reducing scar formation and improving wound healing outcomes. For example, clinical studies using TGF-β3 (a specific isoform) have indicated it may promote more regenerative, less fibrotic healing in surgical wounds. However, direct clinical use of TGF-β itself to treat scars is not common, as its activity typically promotes, rather than reduces, scar tissue. Instead, therapeutic efforts often focus on modulating or inhibiting its signaling. Therefore, while the scientific basis for TGF-β’s involvement in scar tissue is robust, its direct application as a scar treatment is limited and complex, with most interventions aiming to block or adjust its effects rather than use it outright.

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