Angiogenesis in pulmonary fibrosis: too much or not enough?
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.
Department of Medicine, Department of Pathology & Molecular Medicine, St. Joseph's Healthcare, McMaster University, Hamilton, ON, Canada; Firestone Institute for Respiratory Health, St. Joseph's Healthcare, McMaster University, Hamilton, ON, Canada.
Chandru
C
Hanumegowda
Firestone Institute for Respiratory Health, St. Joseph's Healthcare, McMaster University, Hamilton, ON, Canada; Virginia Commonwealth University, Richmond, VA.
Laszlo
L
Farkas
Department of Medicine, Department of Pathology & Molecular Medicine, St. Joseph's Healthcare, McMaster University, Hamilton, ON, Canada; Firestone Institute for Respiratory Health, St. Joseph's Healthcare, McMaster University, Hamilton, ON, Canada. Electronic address: kolbm@mcmaster.ca.
Martin
M
Kolb
D006706:Homeostasis / Q000502:physiology; D006801:Humans; D008168:Lung / Q000098:blood supply*; D055806:Microvessels / Q000503:physiopathology; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D011658:Pulmonary Fibrosis / Q000503:physiopathology*