Human immunodeficiency virus per se exerts atherogenic effects

Oliviero, Ugo; Bonadies, G.; Apuzzi, Valentina; Foggia, Maria; Bosso, Giorgio; Nappa, Salvatore; Valvano, Antonio; Leonardi, Enrico; Borgia, Guglielmo; Castello, Giuseppe; Napoli, Raffaele; Saccà, Luigi

doi:10.1016/j.atherosclerosis.2008.10.012

Cited by 75 publications

(55 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Charakida et al showed that cIMT and FMD were elevated in HIV-infected children, particularly those taking a protease inhibitor (PI)-containing regimen (Charakida et al, 2005). Increased cIMT has been widely reported in HIV-infected populations (Chironi et al, 2003;Hsue et al, 2009a;Hsue et al, 2004;Lorenz et al, 2008;Mercie et al, 2005;Oliviero et al, 2009;van Vonderen et al, 2009), is strongly associated with all-cause mortality in HIV patients (Mangili et al, 2011), and appears to be associated with both HIV infection and HAART regimen (Chironi et al, 2003;Lorenz et al, 2008). Protease inhibitors have been implicated as a mediator of increased cIMT (Maggi et al, 2004).…”

Section: Haart-naïve (N¼20)mentioning

confidence: 94%

“…Protease inhibitors have been implicated as a mediator of increased cIMT (Maggi et al, 2004). Impaired FMD is also widely reported in adult HIV-infected populations and appears to be associated with both HIV-1 RNA levels (Oliviero et al, 2009;Torriani et al, 2008) and HAART (Gupta et al, 2012;Hsue et al, 2009b;Shankar et al, 2005;Stein et al, 2001). Gupta et al reports a significant decrease in FMD in EFV-treated compared to PI-treated subjects after 12 months of treatment (Gupta et al, 2012) and EFV-mediated endothelial dysfunction and arterial stiffening have also been reported in animal models Jamaluddin et al, 2010).…”

Section: Haart-naïve (N¼20)mentioning

confidence: 95%

See 1 more Smart Citation

Efavirenz and ritonavir-boosted lopinavir use exhibited elevated markers of atherosclerosis across age groups in people living with HIV in Ethiopia

Gleason

Caulk

Seifu

et al. 2016

Journal of Biomechanics

View full text Add to dashboard Cite

Section: Haart-naïve (N¼20)mentioning

confidence: 94%

Section: Haart-naïve (N¼20)mentioning

confidence: 95%

Efavirenz and ritonavir-boosted lopinavir use exhibited elevated markers of atherosclerosis across age groups in people living with HIV in Ethiopia

Gleason

Caulk

Seifu

et al. 2016

Journal of Biomechanics

View full text Add to dashboard Cite

“…In the absence of cART, HIV-1 is associated with the development of abnormalities such as increased carotid intimal thickness [Lorenz et al 2008], carotid arterial wall stiffness [Seaberg et al 2010], and abnormalities in vascular compliance and distensibility [Oliviero et al 2009], findings which are associated with atherosclerotic disease. Suppressive cART improves markers of immune activation, inflammation and coagulation, but elevated levels persist despite effective treatment [Neuhaus et al 2010].…”

Section: Accelerated Atherosclerosismentioning

confidence: 99%

HIV stroke risk: evidence and implications

Singer¹,

Valdes-Sueiras

Commins

et al. 2013

Therapeutic Advances in Chronic Disease

View full text Add to dashboard Cite

An estimated 34 million men, women, and children are infected with human immunodeficiency virus type 1 (HIV-1), the virus that causes acquired immunodeficiency syndrome (AIDS). Current technology cannot eradicate HIV-1, and most patients with HIV-1-infection (HIV+) will require lifelong treatment with combined antiretroviral therapy (cART). Stroke was recognized as a complication of HIV-1 infection since the early days of the epidemic. Potential causes of stroke in HIV-1 include opportunistic infections, tumors, atherosclerosis, diabetes, hypertension, autoimmunity, coagulopathies, cardiovascular disease, and direct HIV-1 infection of the arterial wall. Ischemic stroke has emerged as a particularly significant neurological complication of HIV-1 and its treatment due to the aging of the HIV+ population, chronic HIV-1 infection, inflammation, and prolonged exposure to cART. New prevention and treatment strategies tailored to the needs of the HIV+ population are needed to address this issue.

show abstract

“…[1][2][3][4] Antiretroviral therapy may promote premature cardiovascular disease through endothelial dysfunction either indirectly, via protease inhibitor (PI)-induced metabolic disturbances; or directly, via alterations of endothelial cells. [5][6][7][8] Accordingly, several endothelial cell functions, including production of reactive oxygen species (ROS) and secretion of inflammatory cytokines, can be deregulated by short-term exposure (24 to 72 hours) of cultured endothelial cells to ritonavir or other PIs.…”

mentioning

confidence: 99%

Premature Senescence of Vascular Cells Is Induced by HIV Protease Inhibitors

Lefèvre

Auclair

Boccara

et al. 2010

ATVB

View full text Add to dashboard Cite

Objective-To determine whether and how protease inhibitors (PIs) could affect vascular aging. Methods and Results-HIV therapy with PIs is associated with an increased risk of premature cardiovascular disease. The effect of ritonavir and a combination of lopinavir and ritonavir (for 30 days) on senescence, oxidative stress, and inflammation was evaluated in human coronary artery endothelial cells (HCAECs Key Words: endothelial cell Ⅲ PBMC Ⅲ HIV protease inhibitor Ⅲ aging Ⅲ prelamin A Ⅲ statin Ⅲ antioxidants T he increased risk of premature myocardial infarction observed in HIV-infected patients has been attributed to antiretroviral therapy, HIV infection itself, and a synergistic interaction between these factors and other classic cardiovascular risk factors. 1-4 Antiretroviral therapy may promote premature cardiovascular disease through endothelial dysfunction either indirectly, via protease inhibitor (PI)-induced metabolic disturbances; or directly, via alterations of endothelial cells. 5-8 Accordingly, several endothelial cell functions, including production of reactive oxygen species (ROS) and secretion of inflammatory cytokines, can be deregulated by short-term exposure (24 to 72 hours) of cultured endothelial cells to ritonavir or other PIs. 8 -12 The risk of premature cardiovascular events might also result from the accelerated biological aging imposed by antiretroviral therapy and/or HIV itself. [13][14][15][16] Indeed, vascular endothelial cell dysfunction is a feature of the human physiological aging process, 17,18 and syndromes of premature aging are associated with precocious cardiovascular disease. The most striking findings are observed in progeroid syndromes linked to molecular alterations in the prelamin A maturation process. 19 -22 In these genetically determined accelerated aging phenotypes, both vascular endothelial and smooth muscle cells (VSMCs) are altered. 20,23 They exhibit senescent morphological features at the cellular and nuclear levels and aging-related dysfunctions linked to prelamin A accumulation. [23][24][25] Prelamin A accumulation is also observed in VSMCs during physiological aging and in atherosclerotic lesions, where it often colocalized with senescent and degenerate VSMCs. 26 The physiological posttranslational processing of prelamin A is complex, leading to the production of mature lamin A, a ubiquitous protein of the nuclear lamina meshwork. The 2 major steps are catalyzed by a farnesyl transferase, which

show abstract

Human immunodeficiency virus per se exerts atherogenic effects

Cited by 75 publications

References 14 publications

Efavirenz and ritonavir-boosted lopinavir use exhibited elevated markers of atherosclerosis across age groups in people living with HIV in Ethiopia

Efavirenz and ritonavir-boosted lopinavir use exhibited elevated markers of atherosclerosis across age groups in people living with HIV in Ethiopia

HIV stroke risk: evidence and implications

Premature Senescence of Vascular Cells Is Induced by HIV Protease Inhibitors

Contact Info

Product

Resources

About