Angiogenesis in Pulmonary Fibrosis Too Much or Not Enough?
Angiogenesis in Pulmonary Fibrosis Too Much or Not Enough?
复制标题
DOI：
10.1378/chest.11-1962
复制
发表时间：
2012-07-01
期刊：
影响因子：
9.6
通讯作者：
Kolb, Martin
中科院分区：
文献类型：
--
作者：
Hanumegowda, Chandru;Farkas, Laszlo;Kolb, Martin
特发性肺纤维化（IPF）是一种慢性、进行性且通常致命的疾病，其发病机制是多方面的且尚未完全了解。血管重塑的一些细胞和分子机制已被实验探索，很明显，微血管的改变参与了IPF。除其他外，这些可能导致肺动脉高压的发展。为了了解血管完整性和修复的过程，有必要确定IPF中与血管生成相关的因素。血管生成因子和血管生成抑制因子的微妙平衡调节肺中正常生理条件下的血管稳态。尽管早期研究提出IPF与血管生成增加相关，但最近有一些证据表明纤维化肺中的血管生成实际上可能减少，这在该领域的文献中引起了一些争议。因此，本综述讨论了肺纤维化中血管生成的概念，并推测IPF的空间和时间异质性如何解释纤维化肺中血管密度的争议性发现。胸部2012; 142（1）：200-207
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and usually fatal disease, based on a multifaceted and incompletely understood pathogenesis. Some of the cellular and molecular mechanisms of vascular remodeling have been experimentally explored, and it is obvious that alterations of microvessels are involved in IPF. These can, among others, lead to the development of pulmonary hypertension. In order to understand the process of vascular integrity and repair, it is necessary to identify the factors associated with angiogenesis in IPF. A delicate balance of angiogenic and angiostatic factors regulates vessel homeostasis in normal physiologic conditions in the lungs. Although earlier studies have proposed that IPF is associated with an increase of angiogenesis, there is some more recent evidence that angiogenesis in fibrotic lungs may actually be decreased, causing some controversy in the literature in this area. This review, therefore, discusses the concept of angiogenesis in pulmonary fibrosis and speculates on how the spatial and temporal heterogeneity of IPF might explain the controversial findings about vessel density in fibrotic lungs. CHEST 2012; 142(1):200-207