Hein R, Mauch C, Braun-Falco O, Krieg T
Dermatologische Klinik und Poliklinik, Ludwig-Maximilians-Universität München.
Hautarzt. 1988 Feb;39(2):65-71.
Fibrosis is characterized by excessive deposition of connective tissue in the involved organs. Although the prime event in the pathogenesis is still poorly understood, several mechanisms are discussed, which finally result in the activation of fibroblasts. Recent studies have demonstrated that immunocompetent cells play a crucial role during the initial phases of the development of fibrosis. Therefore, several mediators have been characterized, which are secreted by platelets, lymphocytes and macrophages and which can attract fibroblasts, induce proliferation and collagen synthesis in mesenchymal cells. These include PDGF, EGF, TGF--beta and many others. In addition, gamma-interferon has been shown to inhibit chemotaxis of fibroblasts and to reduce collagen mRNA levels. A controlled interaction of all the different mediators is required to guarantee a normal functioning of connective tissue. Alterations in these regulation steps can result in excessive deposition of connective tissue and the development of fibrotic processes.
纤维化的特征是受累器官中结缔组织过度沉积。尽管发病机制中的主要事件仍了解甚少，但已讨论了几种机制，这些机制最终导致成纤维细胞活化。最近的研究表明，免疫活性细胞在纤维化发展的初始阶段起着至关重要的作用。因此，已鉴定出几种由血小板、淋巴细胞和巨噬细胞分泌的介质，它们可吸引成纤维细胞，诱导间充质细胞增殖和胶原蛋白合成。这些介质包括血小板衍生生长因子（PDGF）、表皮生长因子（EGF）、转化生长因子-β（TGF-β）等许多其他因子。此外，γ-干扰素已被证明可抑制成纤维细胞的趋化性并降低胶原蛋白mRNA水平。需要所有不同介质之间的受控相互作用来确保结缔组织的正常功能。这些调节步骤的改变可导致结缔组织过度沉积和纤维化过程的发展。
