HIV protease inhibitor-induced cardiac dysfunction and fibrosis is mediated by platelet-derived TGF-β1 and can be suppressed by exogenous carbon monoxide.

HIV protease inhibitor-induced cardiac dysfunction and fibrosis is mediated by platelet-derived TGF-β1 and can be suppressed by exogenous carbon monoxide.

Human immunodeficiency virus (HIV) infection is an independent risk factor for cardiovascular disease. This risk is magnified by certain antiretrovirals, particularly the protease inhibitor ritonavir, but the pathophysiology of this connection is unknown. We postulated that a major mechanism for ant...

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Bibliographic Details
Main Authors: Jeffrey Laurence, Sonia Elhadad, Tyler Robison, Hunter Terry, Rohan Varshney, Sean Woolington, Shahrouz Ghafoory, Mary E Choi, Jasimuddin Ahamed
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2017-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC5663426?pdf=render

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http://europepmc.org/articles/PMC5663426?pdf=render

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