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HIV-1-Associated Atherosclerosis: Unraveling the Missing Link
J Am Coll Cardiol. 2017 Jun 27;69(25) :3084-3098
PMID: 28641798 PMCID: PMC5512584
AbstractCardiovascular disease, including atherosclerosis and atherosclerosis-associated complications, is an increasing cause of morbidity and mortality in human immunodeficiency virus (HIV) patients in the post-antiretroviral therapy era. HIV alone accelerates atherosclerosis. Antiretroviral therapy; HIV-associated comorbidities, such as dyslipidemia, drug abuse, and opportunistic infections; and lifestyle are risk factors for HIV-associated atherosclerosis. However, our current understanding of HIV-associated atherogenesis is very limited and has largely been obtained from clinical observation. There is a pressing need to experimentally unravel the missing link between HIV and atherosclerosis. Understanding these mechanisms will help to better develop and design novel therapeutic interventions for the treatment of HIV-associated cardiovascular disease. HIV mainly infects T cells and macrophages resulting in the induction of oxidative and endoplasmic reticulum stress, the formation of the inflammasome, and the dysregulation of autophagy. These mechanisms may contribute to HIV-associated atherogenesis. In this review, we will summarize our current understanding and propose potential mechanisms of HIV-associated atherosclerosis.
Notes1558-3597 Kearns, Alison Gordon, Jennifer Burdo, Tricia H Qin, Xuebin T32 MH079785/MH/NIMH NIH HHS/United States R21 AA024984/AA/NIAAA NIH HHS/United States R01 NS082116/NS/NINDS NIH HHS/United States R01 HL130233/HL/NHLBI NIH HHS/United States R01 CA166144/CA/NCI NIH HHS/United States Journal Article Review United States J Am Coll Cardiol. 2017 Jun 27;69(25):3084-3098. doi: 10.1016/j.jacc.2017.05.012.