HIV-related mechanisms in atherosclerosis and cardiovascular diseases

Gibellini, Davide; Borderi, Marco; Clô, Alberto; Morini, Silvia; Miserocchi, Anna; Bon, Isabella; Ponti, Cristina; Re, Maria Carla

doi:10.2459/jcm.0b013e3283619331

Cited by 30 publications

(30 citation statements)

References 164 publications

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“…This suggests that the mechanism by which low pre-ART CD4 is associated with hypertension may not be mediated by chronic immune activation 42,43 . Whereas further data will be required to help elucidate these mechanisms, it could be explained by the possibility that immunodeficiency and immune activation affect hypertension risk through fundamentally distinct pathways 14,44,45 .…”

Section: Discussionmentioning

confidence: 99%

D-Dimer Levels and Traditional Risk Factors Are Associated With Incident Hypertension Among HIV-Infected Individuals Initiating Antiretroviral Therapy in Uganda

Okello

Asiimwe

Kanyesigye

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Objectives We sought to describe blood pressure changes after antiretroviral therapy (ART) initiation and evaluate the association of markers of inflammation with incident hypertension in a cohort of HIV-individuals in Uganda. Methods We used mixed effects linear regression to model changes in systolic blood pressure (BP) over time among a cohort of HIV-infected individuals initiating ART in Uganda. After exclusion of participants with pre-existing hypertension, we identified participants with normal BP throughout follow-up (controls) and those with elevated BP on ≥3 consecutive visits (cases). Prior to ART initiation, participants had testing for lnterleukin-6, kynurenine/tryptophan ratio, lipopolysaccharide, soluble CD14, soluble CD163, and D-dimer and those with viral suppression at six months during ART had repeat tests. We fit logistic regression models to estimate associations between biomarkers and risk of incident hypertension. Results In the entire cohort, systolic BP increased by 9.6 mmHg/year (95% CI 7.3 - 11.8) in the first six months of ART, then plateaued. Traditional factors: male gender (AOR 2.76, 95% CI 1.34-5.68), age (AOR 1.09, 95% CI 1.04-1.13), overweight (AOR 4.48, 95%CI 1.83-10.97), and a CD4 count < 100 cells (AOR 3.08, 95% CI 1.07-8.89) were associated with incident hypertension. After adjusting for these, D-dimer levels at month 6 were inversely associated with incident hypertension (AOR 0.61, 95% CI 0.37-0.99). Although not significant, similar associations were seen with sCD14 and Kynurenine/Tryptophan (K/T) ratio. Conclusion Blood pressure increases early after ART initiation in Ugandans. Traditional risk factors, rather than immune activation were associated with incident hypertension in this population.

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Section: Discussionmentioning

confidence: 99%

D-Dimer Levels and Traditional Risk Factors Are Associated With Incident Hypertension Among HIV-Infected Individuals Initiating Antiretroviral Therapy in Uganda

Okello

Asiimwe

Kanyesigye

et al. 2016

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…55 Nef-mediated transfer of cholesterol to lipid rafts competed with ABCA1-dependent cholesterol efflux through a reduction in cell-surface available ABCA1 and induction of ABCA1 catabolism in the lysosome. As patients with HIV often have atherosclerosis, 56 the interplay between APOL1 risk alleles, HIV and the pathogenesis of atherosclerosis merits further study. Such investigations might indicate that atherosclerosis and glomerulosclerosis are mechanistically related.…”

Section: Insights From Apol1 Mutations In Fsgsmentioning

confidence: 99%

Lipid biology of the podocyte—new perspectives offer new opportunities

2014

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In the past 15 years, major advances have been made in understanding the role of lipids in podocyte biology. First, susceptibility to focal segmental glomerulosclerosis (FSGS) and glomerular disease is associated with an APOL1 sequence variant, is expressed in podocytes and encodes apolipoprotein L1, an important component of HDL. Second, acid sphingomyelinase-like phosphodiesterase 3b encoded by SMPDL3b has a role in the conversion of sphingomyelin to ceramide and its levels are reduced in renal biopsy samples from patients with recurrent FSGS. Furthermore, decreased SMPDL3b expression is associated with increased susceptibility of podocytes to injury after exposure to sera from these patients. Third, in many individuals with membranous nephropathy, autoantibodies against the phospholipase A2 (PLA2) receptor, which is expressed in podocytes, have been identified. Whether these autoantibodies affect the activity of PLA2, which liberates arachidonic acid from glycerophospholipids and modulates podocyte function, is unknown. Fourth, clinical and experimental evidence support a role for ATP-binding cassette sub-family A member 1-dependent cholesterol efflux, free fatty acids and glycerophospolipids in the pathogenesis of diabetic kidney disease. An improved understanding of lipid biology in podocytes might provide insights to develop therapeutic targets for primary and secondary glomerulopathies.

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“…; Gibellini et al. ). Although the mechanisms underlying the HIV‐1‐related vasculopathy are not fully understood, HIV‐1‐associated viral proteins are known to have deleterious effects on the endothelium.…”

Section: Introductionmentioning

confidence: 97%

Effects of HIV-1 gp120 and tat on endothelial cell sensescence and senescence-associated microRNAs

et al. 2018

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The aim of this study was to determine, in vitro, the effects of X4 and R5 HIV‐1 gp120 and Tat on: (1) endothelial cell senescence and (2) endothelial cell microRNA (miR) expression. Endothelial cells were treated with media without and with: R5 gp120 (100 ng/mL), X4 gp120 (100 ng/mL), or Tat (500 ng/mL) for 24 h and stained for senescence‐associated β‐galactosidase (SA‐β‐gal). Cell expression of miR‐34a, miR‐217, and miR‐146a was determined by RT‐PCR. X4 and R5 gp120 and Tat significantly increased (~100%) cellular senescence versus control. X4 gp120 significantly increased cell expression of miR‐34a (1.60 ± 0.04 fold) and miR‐217 (1.52 ± 0.18), but not miR‐146a (1.25 ± 0.32). R5 gp120 significantly increased miR‐34a (1.23 ± 0.07) and decreased miR‐146a (0.56 ± 0.07). Tat significantly increased miR‐34a (1.49 ± 0.16) and decreased miR‐146a (0.55 ± 0.23). R5 and Tat had no effect on miR‐217 (1.05 ± 0.13 and 1.06 ± 0.24; respectively). HIV‐1 gp120 (X4 and R5) and Tat promote endothelial cell senescence and dysregulation of senescence‐associated miRs.

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HIV-related mechanisms in atherosclerosis and cardiovascular diseases

Cited by 30 publications

References 164 publications

D-Dimer Levels and Traditional Risk Factors Are Associated With Incident Hypertension Among HIV-Infected Individuals Initiating Antiretroviral Therapy in Uganda

D-Dimer Levels and Traditional Risk Factors Are Associated With Incident Hypertension Among HIV-Infected Individuals Initiating Antiretroviral Therapy in Uganda

Lipid biology of the podocyte—new perspectives offer new opportunities

Effects of HIV-1 gp120 and tat on endothelial cell sensescence and senescence-associated microRNAs

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