Abstract
Sir, The clinical management of keloids and hypertrophic scars remains problematic. The numerous treatments currently available ‐ including surgical excision, steroid injection, radiation therapy, laser, and pressure therapy, among others ‐ underscore the poor comprehension of the molecular processes underlying abnormal scars [1]. It is nonetheless anticipated that a better understanding of the pathophysiology of keloid scarring holds great promise for developing novel therapeutic strategies. In this regard, upregulation of transforming growth factor beta (TGF-b )i s deemed to play a crucial role in the excessive accumulation of type I collagen in keloids [2]. Additionally, a hyperexpression of matrix metalloproteinase-2 (MMP-2, gelatinase B) by keloid fibroblasts may account for the invasive nature of this lesion [3]. These findings may logically lead to the hypothesis that reduction in collagen accumulation, as well as inhibition of MMP-2 production, may represent a novel therapeutic target for treating keloids. We speculate that such a therapeutic effect could be reached by topic administration of halofuginone hydrobromide, a low molecular weight plant alkaloid. There are at least three lines of evidence supporting the potential usefulness of halofuginone for keloid management. First, halofuginone has been found to inhibit fibroblast proliferation, type I collagen gene expression as well as TGF-b signaling pathway [4]. Second, this compound may potently reduce the percentage of active MMP-2 [5], thus potentially contrasting the expansion and the invasive nature of keloids. Finally, halofuginone has a striking antiangiogenic activity [6] that may reduce keloid neovascularization. Given that topical preparations of halofuginone hydrobromide are currently being developed [7], clinical studies are urgently needed to investigate the clinical efficacy of this compound as a treatment option for abnormal scar tissue.
Published Version
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