2016 Wylie Scholar
- Angela Ramirez
- Oct 9
- 2 min read
Ryan McEnaney, MD
Assistant Professor of Surgery
University of Pittsburgh School of Medicine
VA Pittsburgh Healthcare System
Wylie Research Focus: To improve collateral artery development, known as arteriogenesis
Date Awarded: 2016
“The focus of my lab is to better understand how arteries build collateral or “backup” blood vessels that take over when an artery is blocked. This knowledge can help in the development of alternatives to surgery for patients with blood flow blockages.”
Dr. Ryan McEnaney received the 2016 Wylie Scholar Award for his research that aims to improve collateral artery development, known as arteriogenesis. His lab has demonstrated that growing better collateral circulation is possible. The physical forces of flowing blood acting on the vessel wall are important determinants of the size and capacity that collateral vessels will achieve. Dr. McEnaney seeks to understand the molecular signals in the vessel wall that communicate change in flowing blood. Identifying the secondary molecular messages could lead to pharmaceutical therapies to improve collateral circulation for patients unable to undergo surgery.
Additionally, for pre-existing arteries to grow into collaterals, the matrix structure must be reorganized and sometimes rebuilt. Unfortunately, some of the critical components of an artery’s structure are limited – created in early life but seemingly irreplaceable if destroyed. Key to arterial remodeling is the careful reorganization and redistribution of certain structural components so that the vessel may enlarge, but not deteriorate. Dr. McEnaney’s lab has been using advanced imaging modalities to investigate the extracellular matrix reorganization of enlarging collateral vessels. Understanding these processes have implications for not just arteriogenesis and collateral development, but also arterial aneurysmal disease. With the work accomplished through the Wylie Award’s support, Dr. McEnaney has been awarded federal funding via VA CDA mechanism.
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