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Angiogenesis in Pulmonary FibrosisAngiogenesis in Pulmonary Fibrosis: Too Much or Not Enough?

Chandru Hanumegowda, PhD; Laszlo Farkas, MD; Martin Kolb, MD, PhD
Author and Funding Information

From the Department of Medicine, Department of Pathology & Molecular Medicine (Drs Hanumegowda and Kolb), Firestone Institute for Respiratory Health (Drs Hanumegowda, Farkas, and Kolb), St. Joseph’s Healthcare, McMaster University, Hamilton, ON, Canada; and the Virginia Commonwealth University (Dr Farkas), Richmond, VA.

Correspondence to: Martin Kolb, MD, PhD, Departments of Medicine, Pathology, & Molecular Medicine, McMaster University, Firestone Institute for Respiratory Health, 50 Charlton Ave E, Room T2131, Hamilton, ON, L8N 4A6, Canada; e-mail: kolbm@mcmaster.ca

Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Kolb received consultancy fees from GlaxoSmithKline, Boehringer Ingelheim GmbH, and InterMune, and an unrestricted research grant from GlaxoSmithKline. Drs Hanumegowda and Farkas have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Funding/Support: This study was funded by a Research Fellowship of the Deutsche Forschungsgemeinschaft for Dr Farkas, funded by the Canadian Institute for Health Research.


Funding/Support: This study was funded by a Research Fellowship of the Deutsche Forschungsgemeinschaft for Dr Farkas, funded by the Canadian Institute for Health Research.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2012;142(1):200-207. doi:10.1378/chest.11-1962
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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.

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