Seifert Oliver, Mrowietz Ulrich
Department of Dermatology, County Hospital Ryhov, Jonkoping 55185, Sweden.
Arch Dermatol Res. 2009 Apr;301(4):259-72. doi: 10.1007/s00403-009-0952-8. Epub 2009 Apr 10.
Wound healing is a fundamental complex-tissue reaction leading to skin reconstitution and thereby ensuring survival. While, fetal wounds heal without scarring, a normal "fine line" scar is the clinical outcome of an undisturbed wound healing in adults. Alterations in the orchestrated wound healing process result in hypertrophic or keloid scarring. Research in the past decades attempted to identify genetic, cellular, and molecular factors responsible for these alterations. These attempts lead to several new developments in treatments for keloids, such as, imiquimod, inhibition of transforming growth factor beta, and recombinant interleukin-10. The urgent need for better therapeutics is underlined by recent data substantiating an impaired quality of life in keloid and hypertrophic scar patients. Despite the increasing knowledge about the molecular regulation of scar formation no unifying theory explaining keloid development has been put forward until today. This review aims to give an overview about the genetic and molecular background of keloids and focus of the current research on keloid scarring with special emphasis on new forthcoming treatments. Clinical aspects and the spectrum of scarring are summarized.
伤口愈合是一种基本的复杂组织反应，可导致皮肤重建，从而确保生存。虽然胎儿伤口愈合不会留下疤痕，但正常的“细线状”疤痕是成人伤口正常愈合的临床结果。精心编排的伤口愈合过程发生改变会导致增生性或瘢痕疙瘩性瘢痕形成。过去几十年的研究试图确定导致这些改变的遗传、细胞和分子因素。这些尝试带来了瘢痕疙瘩治疗方面的一些新进展，例如咪喹莫特、转化生长因子β抑制以及重组白细胞介素-10。最近的数据证实瘢痕疙瘩和增生性瘢痕患者的生活质量受损，这凸显了对更好治疗方法的迫切需求。尽管对瘢痕形成的分子调节的了解日益增加，但直到今天，尚未提出一个统一的理论来解释瘢痕疙瘩的形成。本综述旨在概述瘢痕疙瘩的遗传和分子背景以及当前瘢痕疙瘩瘢痕形成研究的重点，特别强调即将出现的新治疗方法。总结了临床方面和瘢痕形成的范围。
