How HIV protease inhibitors promote atherosclerotic lesion formationThomas, Candice M; Smart, Eric JCurrent Opinion in Lipidology: October 2007 - Volume 18 - Issue 5 - p 561–565 doi: 10.1097/MOL.0b013e3282ef604f Atherosclerosis: cell biology and lipoproteins Abstract Author Information Purpose of review One of the aims of this review is to summarize recent clinical approaches used to determine the role of HIV protease inhibitors in the development of cardiovascular disease. Another aim is to discuss possible molecular mechanisms whereby HIV protease inhibitors may promote atherogenesis. Recent findings Several clinical studies have recently used ultrasonography to demonstrate increased intimal medial thickness and alterations in the structural characteristics of epi-aortic lesions in patients receiving HIV protease inhibitors. Molecular studies have indicated that several mechanisms are likely involved in mediating the effects of protease inhibitors. Possible mechanisms include inhibition of the proteasome, increased CD36 expression in macrophage, inhibition of lipoprotein lipase-mediated lipolysis, decreased adiponectin levels, and dysregulation of the NF-κB pathway. Summary The currently available data strongly suggest that HIV protease inhibitors negatively impact the cardiovascular system. As is often the case with complex diseases like atherosclerosis it appears that HIV protease inhibitors affect the cardiovascular system through several distinct mechanisms by affecting various components of the arterial wall directly or indirectly by influencing lipoprotein and glucose metabolism of the body. Department of Pediatrics and the Kentucky Pediatric Research Institute, University of Kentucky, Lexington, Kentucky, USA Correspondence to Eric J. Smart, University of Kentucky, Department of Pediatrics, 423 Sanders-Brown, 800 Limestone Street, Lexington, KY 40536-0230, USA Tel: +1 859 323 6412; fax: +1 859 257 2120; e-mail: email@example.com © 2007 Lippincott Williams & Wilkins, Inc.