Shaw Tanya J, Kishi Kazuo, Mori Ryoichi
St George's, University of London, UK.
Endocr Metab Immune Disord Drug Targets. 2010 Dec;10(4):320-30. doi: 10.2174/1871530311006040320.
Skin fibrosis, in its mildest form, may present only a minor aesthetic problem, but in the most severe cases it can lead to debilitating pathologies of the skin, for example keloid and hypertrophic scars, and systemic sclerosis. In recent years, extensive basic research aimed at understanding the molecular mechanisms underlying fibrosis has revealed an impressive but baffling number of genes, molecules, and cell types that may contribute to this problem. However, one recurring and consistent theme in these studies is that inflammatory cells and their secreted mediators appear to be leading culprits in activating dermal fibroblasts to become fibrotic. This review will first describe the histology of normal versus fibrotic skin, and will also describe the process of wound repair, a primary cause of skin fibrosis. We will then focus on what is currently known about the molecular mechanisms underlying skin fibrosis, with particular attention paid to how inflammation contributes. Finally, current treatment strategies and emerging therapeutic targets will be discussed.
皮肤纤维化，在其最轻微的形式下，可能仅表现为一个较小的美学问题，但在最严重的情况下，它会导致使人衰弱的皮肤病变，例如瘢痕疙瘩和增生性瘢痕，以及系统性硬化症。近年来，旨在了解纤维化潜在分子机制的广泛基础研究揭示了数量众多、令人印象深刻但又令人困惑的可能导致这一问题的基因、分子和细胞类型。然而，这些研究中一个反复出现且一致的主题是，炎症细胞及其分泌的介质似乎是激活真皮成纤维细胞使其发生纤维化的主要元凶。本综述将首先描述正常皮肤与纤维化皮肤的组织学，还将描述伤口修复过程，这是皮肤纤维化的一个主要原因。然后，我们将专注于目前已知的皮肤纤维化潜在分子机制，特别关注炎症是如何起作用的。最后，将讨论当前的治疗策略和新出现的治疗靶点。
