Atherosclerosis is a leading cause of heart attacks and stroke. The narrowing of blood vessels that is caused by atherosclerosis can be treated with angioplasty or stenting to improve blood flow. However, the stenting process induces deleterious remodeling of the blood vessel that can increase thrombosis risk, limiting the use of this strategy. In an article published in the Journal of Clinical Investigation , a research team led by Ziad Ali of the Columbia University Medical Center now provides new insights into the pathological remodeling that occurs following blood vessel stenting. In patients, they show that a gene network regulated by the antioxidant enzyme glutathione peroxidase-1 (GPX1) was downregulated in atherosclerotic plaques and a gene variant in the receptor tyrosine kinase ROS1 was associated with adverse effects of stenting. In a mouse model, loss of the antioxidant GPX1 promoted both oxidative and reductive stress, which in turn led to elevated ROS1 activity. Their study suggests ROS1 merits further exploration as a therapeutic target to improve the treatment of flow-limiting atherosclerosis.
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Title
Oxido-reductive regulation of vascular remodeling by receptor tyrosine kinase ROS1
Author Contact
Ziad Ali
Columbia University Medical Center, New York, NY, USA
Phone: 6464501870
Fax: 2123423857
E-mail: zaa2112@columbia.edu
View this article at: http://www.jci.org/articles/view/77484?key=e4b9a9da5d2bb7f78455
Accompanying Commentary Title
Limiting reductive stress for treating in-stent stenosis: the heart of the matter?
Judy de Haan
Baker Heart Institute
Melbourne, AUS
judy.dehaan@bakeridi.edu.au
Phone 1: 56-4321-7890
View this article at: http://www.jci.org/articles/view/79423?key=9b0b76f89a1d06ddaea5
Journal of Clinical Investigation