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Am J Physiol Lung Cell Mol Physiol (March 23, 2007). doi:10.1152/ajplung.00378.2006
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Submitted on September 25, 2006
Accepted on March 15, 2007

Perspectives on Endothelial-Mesenchymal Transition: Potential Contribution to Vascular Remodeling in Chronic Pulmonary Hypertension

Enrique Arciniegas1, Maria G. Frid2, Ivor Samuel Douglas3, and Kurt R. Stenmark4*

1 Universidad Central de Venezuela, Caracas, Venezuela
2 Pediatric Critical Care/Dev Lung Bio Lab, University of Colorado Health Science Center, Denver, Colorado, United States
3 Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, denver, Colorado, United States
4 Pediatric Critical Care/Developmental Lung Biology, University of Colorado, Health Science Center, Denver, United States

* To whom correspondence should be addressed. E-mail: kurt.stenmark{at}uchsc.edu.

All forms of pulmonary hypertension are characterized by structural changes in pulmonary arteries. Increased numbers of cells expressing {alpha}-SM-actin is a near universal finding in the remodeled artery. Traditionally, it was assumed that resident SMC were the exclusive source of these newly appearing {alpha}-SM-actin-expressing cells. However, rapidly emerging experimental evidence suggests other, alternative cellular sources of these cells. One possibility is that endothelial cells can transition into mesenchymal cells expressing {alpha}-SM-actin, and that this process contributes to the accumulation of SM-like cells in vascular pathologies. We review the evidence that endothelial-mesenchymal transition is an important contributor to cardiac and vascular development as well as to pathophysiologic vascular remodeling. Recent work has provided evidence for the role of TGF-{beta}, Wnt, and Notch signaling in this process. The potential roles of matrix metalloproteinases and serine proteases are also discussed. Importantly, endothelial-mesenchymal transition may be reversible. Thus insights into the mechanisms controlling endothelial-mesenchymal transition are relevant to vascular remodeling and are important as we consider new therapies aimed at reversing pulmonary vascular remodeling.




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