Semin Respir Crit Care Med 2006; 27(6): 589-599
DOI: 10.1055/s-2006-957331
Copyright © 2006 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA.

Inflammation and Angiogenesis in Fibrotic Lung Disease

Michael P. Keane1 , Robert M. Strieter2 , Joseph P. Lynch1  III , John A. Belperio1
  • 1Division of Pulmonary and Critical Care Medicine, UCLA David Geffen School of Medicine at UCLA, Los Angeles, California
  • 2Department of Medicine, University of Virginia, Charlottesville, Virginia
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Publication History

Publication Date:
29 December 2006 (online)

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ABSTRACT

The pathogenesis of pulmonary fibrosis is poorly understood. Although inflammation has been presumed to have an important role in the development of fibrosis this has been questioned recently, particularly with regard to idiopathic pulmonary fibrosis (IPF). It is, however, increasingly recognized that the polarization of the inflammatory response toward a type 2 phenotype supports fibroproliferation. Increased attention has been on the role of noninflammatory structural cells such as the fibroblast, myofibroblast, epithelial cell, and endothelial cells. Furthermore, the origin of these cells appears to be multifactorial and includes resident cells, bone marrow-derived cells, and epithelial to mesenchymal transition. Increasing evidence supports the presence of vascular remodeling in fibrotic lung disease, although the precise role in the pathogenesis of fibrosis remains to be determined. Therefore, the pathogenesis of pulmonary fibrosis is complex and involves the interaction of multiple cell types and compartments within the lung.

REFERENCES

Michael P KeaneM.D. 

UCLA, Department of Medicine, Division of Pulmonary and Critical Care Medicine

900 Veteran Ave., 14-154 Warren Hall, Los Angeles, CA 90095-1922

Email: mpkeane@mednet.ucla.edu