Angiogenesis in Pulmonary Fibrosis Too Much or Not Enough?

被引:134
作者
Hanumegowda, Chandru [1 ]
Farkas, Laszlo [2 ]
Kolb, Martin [1 ]
机构
[1] McMaster Univ, Dept Med, Firestone Inst Resp Hlth, Dept Pathol & Mol Med, Hamilton, ON L8N 4A6, Canada
[2] Virginia Commonwealth Univ, Richmond, VA USA
关键词
ENDOTHELIAL GROWTH-FACTOR; BRONCHOALVEOLAR LAVAGE FLUID; CXC CHEMOKINES; LUNG FIBROSIS; MATRIX METALLOPROTEINASES; TISSUE INHIBITOR; EXPRESSION; HYALURONAN; VEGF; ENDOSTATIN;
D O I
10.1378/chest.11-1962
中图分类号
R4 [临床医学];
学科分类号
100218 [急诊医学];
摘要
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
引用
收藏
页码:200 / 207
页数:8
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