New molecular medicine-based scar management strategies

Abstract

Keloids and hypertrophic scars are prevalent disabling conditions with still suboptimal treatments. Basic science and molecular-based medicine research has contributed to unravel new bench-to-bedside scar therapies, and to dissect the complex signaling pathways involved. Peptides such as transforming growth factor beta (TGF-β) superfamily, with SMADs, Ski, SnoN, Fussels, endoglin, DS-Sily, Cav-1p, AZX100, thymosin-β4 and other related molecules may emerge as targets to prevent and treat keloids and hypertrophic scars. The aim of this review is to describe the basic complexity of these new molecular scar management strategies, and point out new fibrosis research lines.

Transforming growth factor β3 attenuates the development of radiation-induced pulmonary fibrosis in mice by decreasing fibrocyte recruitment and regulating IFN-γ/IL-4 balance

“…The expression of TGF-␤1 was shown to be upregulated in many tissues in the development of fibrosis, while the expression of TGF-␤3 was not influenced in such processes [18,19]. Unlike the profibrotic function of TGF-␤1, TGF-␤3 showed the potential anti-fibrotic properties especially in scar-less wound healing, suggesting a different mechanism to inhibit matrix degradation as opposed to TGF-␤1 [20,21]. The overexpression of TGF-␤3 in rat lungs tended to initiate a transient and non-progressive fibrogenic response and result in non-fibrotic tissue repair than overexpression of TGF-␤1 [22].…”

Up-to-date approach to manage keloids and hypertrophic scars: A useful guide

“…Furthermore, increased number of mast cells have been associated with enhanced HIF-1α (hypoxia inducible factor-1α), VEGF (vascular endothelial growth factor) and PAI-1 (plasminogen activator inhibitor-1) expression, all well known fibrosis promoters. TGF-β signaling with preponderance of TGF-β1 or 2 expression due to alteration of POMC (proopiomelanocortin) gene expression among other mechanisms and epithelial-to-mesenchymal transition have also been shown to play a major role in keloid formation [10,11]. Increased interleukin-6 (IL-6), PDGF (platelet derived growth factor), α 1 β 1 -integrin and Ig A, G and M expression have all also been linked to keloid pathogenesis [3].…”

Baicalein attenuates hypertrophic scar formation via inhibition of the transforming growth factor‐β/Smad2/3 signalling pathway

“…Under such circumstances, fibroblasts stay activated for a prolonged period of time, resulting in massive collagen secretion and fibroproliferative disorders . One of the key cytokines regulating this fibrotic process is transforming growth factor (TGF)‐β, which has been reported to have a remarkable impact on the recruitment and activation of fibroblasts through TGF‐β/Smad signalling …”

“…12 One of the key cytokines regulating this fibrotic process is transforming growth factor (TGF)-b, which has been reported to have a remarkable impact on the recruitment and activation of fibroblasts through TGF-b/Smad signalling. [13][14][15] Baicalein, or 5,6,7-trihydroxyflavone, is a type of flavonoid originally isolated from the roots of Scutellaria baicalensis and Scutellaria lateriflora. This compound has been shown to possess a variety of biological characteristics, including antioxidative 16 and anti-inflammatory effects, 17 tumour growth inhibition 18 and protection of ischaemia/reperfusion injury.…”