Tzouvelekis Argyris, Anevlavis Stavros, Bouros Demosthenes
Department of Pneumonology, Medical School, Democritus University of Thrace, Greece.
Respir Res. 2006 May 25;7(1):82. doi: 10.1186/1465-9921-7-82.
The past ten years parallels have been drawn between the biology of cancer and pulmonary fibrosis. The unremitting recruitment and maintenance of the altered fibroblast phenotype with generation and proliferation of immortal myofibroblasts is reminiscent with the transformation of cancer cells. A hallmark of tumorigenesis is the production of new blood vessels to facilitate tumor growth and mediate organ-specific metastases. On the other hand several chronic fibroproliferative disorders including fibrotic lung diseases are associated with aberrant angiogenesis. Angiogenesis, the process of new blood vessel formation is under strict regulation determined by a dual, yet opposing balance of angiogenic and angiostatic factors that promote or inhibit neovascularization, respectively. While numerous studies have examined so far the interplay between aberrant vascular and matrix remodeling the relative role of angiogenesis in the initiation and/or progression of the fibrotic cascade still remains elusive and controversial. The current article reviews data concerning the pathogenetic role of angiogenesis in the most prevalent and studied members of ILD disease-group such as IIPs and sarcoidosis, presents some of the future perspectives and formulates questions for potential further research.
在过去十年中，人们对癌症生物学和肺纤维化进行了比较。持续招募并维持改变后的成纤维细胞表型，以及永生肌成纤维细胞的生成和增殖，让人联想到癌细胞的转变。肿瘤发生的一个标志是产生新血管以促进肿瘤生长并介导器官特异性转移。另一方面，包括纤维化肺病在内的几种慢性纤维增生性疾病与异常血管生成有关。血管生成，即新血管形成的过程，受到严格调控，这取决于分别促进或抑制新血管形成的血管生成因子和血管生成抑制因子的双重但相反的平衡。尽管到目前为止已有大量研究探讨了异常血管重塑与基质重塑之间的相互作用，但血管生成在纤维化级联反应的起始和/或进展中的相对作用仍然难以捉摸且存在争议。本文回顾了有关血管生成在间质性肺疾病（ILD）疾病组中最常见且研究最多的成员（如特发性间质性肺炎（IIP）和结节病）发病机制中的作用的数据，提出了一些未来展望，并提出了有待进一步研究的问题。
