From the Guidelines
The answer is (a) transforming growth factor-β. Keloid formation is associated with increased levels of transforming growth factor-β (TGF-β), which plays a crucial role in the pathogenesis of these abnormal scars. Although the provided study 1 discusses various growth factors such as platelet-derived growth factor, basic fibroblast growth factor, and epidermal growth factor in the context of leiomyoma research, it does not directly address keloid formation. However, based on the general understanding of keloid pathogenesis, TGF-β is known to promote excessive collagen synthesis and deposition by fibroblasts, inhibit collagen degradation, and stimulate fibroblast proliferation. Some key points to consider in keloid formation include:
- The role of TGF-β in promoting excessive scarring
- The dysregulation of TGF-β signaling in keloids, with overexpression of TGF-β1 and TGF-β2 isoforms and decreased expression of TGF-β3
- The increased sensitivity of keloid fibroblasts to TGF-β stimulation compared to normal fibroblasts While other growth factors like PDGF, EGF, bFGF, and TNF-α may play roles in wound healing, the most consistently implicated growth factor in keloid pathogenesis is TGF-β, as supported by the highest quality and most recent studies, although not directly cited here, the provided study 1 does not provide direct evidence for keloid formation.
From the Research
Keloid Formation and Growth Factors
- Keloid formation has been associated with an increased amount of certain growth factors, including:
Role of TGF-β in Keloid Formation
- TGF-β plays a key role in keloid formation, with studies showing that it stimulates DNA synthesis and collagen production in keloid-derived fibroblasts 4
- Keloid fibroblasts exhibit an altered response to TGF-β, with increased sensitivity to its effects 5
- TGF-β has been shown to increase the expression of collagen and other extracellular matrix components in keloid fibroblasts 2, 4