Pathophysiological Factors Contributing to Keloid Formation

蟹足腫形成之病理生理因子

葉發來(Fa-Lai Yeh)

《Formosan Journal of Surgery》 43卷1期 (2010/02) Pp. 1-6

https://doi.org/10.29833/FJS.201002.0001

摘要

正常之傷口癒合會導致蟹足腫。目前蟹足腫的治療對醫師們而言，仍是相當困難且具挑戰性。若我們能對這種疾病之成因有更完整的了解，將有助於成功治療方式之開發。本文乃綜述目前我們對蟹足腫成因之了解。文獻上以及我們的研究結果顯示，與來自正常組織的纖維母細胞相比，蟹足腫纖維母細胞呈現較強的生長潛力，以及可以產生較多量的膠原蛋白。此外，我們的研究結果亦顯示，與正常的纖維母細胞相比，蟹足腫纖維母細胞產生較少量的、能參與以及調控發炎反應的物質，包括MCP-1、PGE2、MMP-1、MMP-2以及TIMP-2。近來的文獻也顯示，蟹足腫的組織產生過量的TGF-β，且TGF-β的產生調控也不正常。以上這些在傷口癒合程序中所發生的改變，可能導致延遲的、延續的發炎反應，以及皮膚傷口膠原蛋白的堆積，而形成難纏的蟹足腫。

並列摘要

Keloid formation occurs following an abnormal wound healing. It represents a significant therapeutic challenge to physicians. A better understanding of the pathophysiologic processes underlying keloid formation may help in the development of more successful therapeutic interventions. This article delineates current information on the pathogenesis of keloids. Results reported in the literature and obtained from our studies showed that keloid-derived fibroblasts demonstrated a higher growth potential and produced higher levels of procollagen than those produced by control-derived fibroblasts. In addition, our results also showed a decreased production of inflammatory mediators of MCP-1, PGE2, MMP-1, MMP-2 and TIMP-2 by keloid-derived fibroblasts as compared with normal skin-derived fibroblasts. Furthermore, current literature also indicates that the growth factor TGF-ß is overproduced and poorly regulated in keloid tissue. These alterations in the wound healing process may result in delayed and prolonged activation of injuryinduced inflammation as well as imbalance in the extracellular matrix formation and degradation that may contribute to excess deposition of collagen in skin lesions and lead to keloid formation.

並列關鍵字

keloid ； pathophysiology