Endothelial Progenitor Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis: An Evolving Concept

Abstract

The current data suggest that inadequate levels of early EPCs may potentially contribute to suppressed repair and recovery of the damaged pulmonary endothelium and thereby may drive the sequence of events in profibrogenic direction. Increased VEGFmRNA levels in the clinical context of IPF may represent a compensatory mechanism to overcome reduced EPCs levels.