Cardiometabolic and vascular effects of treatment with a fixed-dose combination anti-retroviral drug containing nucleoside and non-nucleoside reverse transcriptase inhibitors (NRTI s and NNRTI s ) in adult rats

Strijdom, Hans; Goswami, Nandu; Boever, Patrick De; Westcott, C.; Ogundipe, T P; Everson, Frans; Genis, Amanda

doi:10.1016/j.atherosclerosis.2016.07.791

Cited by 4 publications

(6 citation statements)

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“…showed that the levels of several biomarkers of vascular inflammation (sVCAM‐1, MCP‐1 and von Willebrand factor) were lowered by short‐term HAART. In our laboratory, treatment with a fixed‐dose combination of Emtricitabine–Tenofovir–Efavirenz improved vascular function in the aortas of rats, which was associated with increased eNOS expression . In 2013, the WHO published new recommendations on first‐line ART regimens .…”

Section: Antiretroviral Therapy and Endothelial Dysfunctionmentioning

confidence: 99%

“…In HIV-positive human participants who were either treatment na€ ıve or had not used ART for at least 6 months, ART seemed to lower asymmetric dimethylarginine (ADMA) levelsa novel marker of endothelial dysfunction [87]; in addition, Francisci et al [88] showed that the levels of several biomarkers of vascular inflammation (sVCAM-1, MCP-1 and von Willebrand factor) were lowered by short-term HAART. In our laboratory, treatment with a fixed-dose combination of Emtricitabine-Tenofovir-Efavirenz improved vascular function in the aortas of rats, which was associated with increased eNOS expression [89]. In 2013, the WHO published new recommendations on first-line ART regimens [90].…”

Section: Antiretroviral Therapy and Endothelial Dysfunctionmentioning

confidence: 99%

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Vascular endothelial dysfunction in the wake of HIV and ART

et al. 2018

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Mounting evidence points to increased rates of cardiovascular disease (CVD) among people living with HIV/AIDS (PLWHA). Endothelial dysfunction (loss of endothelium-dependent vascular relaxation in response to provasodilatory stimuli) constitutes an early pathophysiological event in atherogenesis and CVD. Both HIV-1 infection and antiretroviral therapy (ART) are implicated in the development of endothelial dysfunction; however, conclusions are frequently drawn from associations shown in epidemiological studies. In this narrative review of mainly in vitro and animal studies, we report on the current understanding of how various HIV-1 proteins, HIV-1-induced proinflammatory cytokines and common antiretroviral drugs directly impact vascular endothelial cells. Proposed cellular mechanisms underlying the switch to a dysfunctional state are discussed, including oxidative stress, impaired expression and regulation of endothelial nitric oxide (NO) synthase (eNOS) and increased expression of vascular adhesion molecules. From the literature, it appears that increased reactive oxygen species (ROS) production, linked to decreased NO bioavailability and ensuing endothelial dysfunction, may be proposed as a putative final common pathway afflicting the vascular endothelium in PLWHA. The HIV-1-proteins Tat, Gp120 and Nef in particular, the proinflammatory cytokine, TNF-α, and the antiretroviral drugs Efavirenz and Lopinavir, most commonly postulated to be primary causal agents of endothelial dysfunction, are also discussed. We conclude that, despite existing evidence from basic research papers, a significant gap remains in terms of the exact underlying cellular mechanisms involved in HIV-1 and ART induced endothelial dysfunction. Bridging this gap could help pave the way for future strategies to prevent and treat early cardiovascular changes in PLWHA.

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Section: Antiretroviral Therapy and Endothelial Dysfunctionmentioning

confidence: 99%

Section: Antiretroviral Therapy and Endothelial Dysfunctionmentioning

confidence: 99%

Vascular endothelial dysfunction in the wake of HIV and ART

et al. 2018

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“…NRF2 expression increases show an antioxidant response and balance restoration. NRF2, an antioxidant, regulates metabolic balance and eliminates lipid buildup and oxidative stress . SNP activated NRF2 due to its antioxidant action, as evidenced by increased mRNA levels of NRF2 and HO-1 in the kidneys of diabetic rats …”

Section: Discussionmentioning

confidence: 99%

Exploring the NRF2/HO-1 and NF-κB Pathways: Spirulina Nanoparticles as a Novel Approach to Combat Diabetic Nephropathy

Althobaiti,

Taher,

Ahmed Alkeridis

et al. 2024

ACS Omega

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Arthrospira platensis has been the subject of plentiful studies due to its purported health advantages; nevertheless, additional investigation is required to determine whether several chronic diseases may be treated or avoided with its nanoform. Therefore, we set out to examine A. platensis nanoparticles (SNPs) to protect against kidney impairment caused by Streptozotocin (STZ) in diabetic rats, precisely focusing on its effect and the cellular intracellular pathways involved. Male Wistar rats were assigned into four groups: Group 1 was set as control, comprising the normal rats; group 2 was administered SNPs (0.5 mg/kg BW, once/day) orally for 84 consecutive days; group 3, STZ-diabetic rats were injected with STZ (65 mg/kg BW); and group 4, in which the diabetic rats were treated with SNPs. After inducing diabetes in rats for 84 days, the animals were euthanized. The results disclosed that SNP treatment substantially (P < 0.05) improved the glucose and glycated hemoglobin levels (HbA1c %), insulin, C-peptide, and cystatin C deterioration in diabetic rats. Furthermore, SNP administration significantly lowered (P < 0.05) nitric oxide (NO) and malondialdehyde (MDA) levels in renal tissue and enhanced kidney function metrics, as well as improved the antioxidant capacity of the renal tissue. In addition, oral SNPs overcame the diabetic complications concerning diabetic nephropathy, indicated by downregulation and upregulation of apoptotic and antiapoptotic genes, respectively, along with prominent modulation of the antiangiogenic marker countenance level, improving kidney function. SNP modulated the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 (NRF2/HO-1) pathways and inhibited the nuclear factor-κB (NF-κB) expression, strengthening the SNP pathways in alleviating diabetic nephropathy. The histopathology results corroborated the obtained biochemical and molecular observations, suggesting the therapeutic potential of SNPs in diabetic nephropathy via mechanisms other than its significant antioxidant and hypoglycemic effects, including modulation of antiangiogenic and inflammatory mediators and the NRF2/HO-1 pathways.

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“…257 The protease inhibitors such as ritonavir-boosted darunavir, lopinavir, and atazanavir are largely considered to be the most cardiotoxic, causing hyperlipidemia, insulin resistance, oxidative stress, and cellular senescence that together contribute to increased CVD risk with long-term use. 251,258,259 Nevertheless, combined ART regimens provide substantial benefit to PLWH that includes improved vascular function in previously treatment-naive PLWH due to their effective suppression of the HIV virus. In fact, preclinical evidence has also indicated that ART regimens (eg, emtricitabine-tenofovir-efavirenz) improve aortic vascular function by increasing eNOS expression.…”

Section: Art Regimens and Accelerated Vascular Aging In Plwhmentioning

confidence: 99%

“…In fact, preclinical evidence has also indicated that ART regimens (eg, emtricitabine-tenofovir-efavirenz) improve aortic vascular function by increasing eNOS expression. 260,261 Accordingly, the Strategies for Management of Antiretroviral Therapy indicated that viral suppression by ART was associated with reduced CVD risk. 262 A recent review and meta-analysis indicated that, overall, ART use contributes to decreased endothelial activation as evidenced by decreased VCAM-1 and ICAM-1.…”

Section: Mechanisms Of Accelerated Vascular Aging In Hivmentioning

confidence: 99%

Exercise to Prevent Accelerated Vascular Aging in People Living With HIV

Jones,

Robinson,

Beach

et al. 2024

Circulation Research

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Given advances in antiretroviral therapy, the mortality rate for HIV infection has dropped considerably over recent decades. However, people living with HIV (PLWH) experience longer life spans coupled with persistent immune activation despite viral suppression and potential toxicity from long-term antiretroviral therapy use. Consequently, PLWH face a cardiovascular disease (CVD) risk more than twice that of the general population, making it the leading cause of death among this group. Here, we briefly review the epidemiology of CVD in PLWH highlighting disparities at the intersections of sex and gender, age, race/ethnicity, and the contributions of social determinants of health and psychosocial stress to increased CVD risk among individuals with marginalized identities. We then overview the pathophysiology of HIV and discuss the primary factors implicated as contributors to CVD risk among PLWH on antiretroviral therapy. Subsequently, we highlight the functional evidence of premature vascular dysfunction as an early pathophysiological determinant of CVD risk among PLWH, discuss several mechanisms underlying premature vascular dysfunction in PLWH, and synthesize current research on the pathophysiological mechanisms underlying accelerated vascular aging in PLWH, focusing on immune activation, chronic inflammation, and oxidative stress. We consider understudied aspects such as HIV-related changes to the gut microbiome and psychosocial stress, which may serve as mechanisms through which exercise can abrogate accelerated vascular aging. Emphasizing the significance of exercise, we review various modalities and their impacts on vascular health, proposing a holistic approach to managing CVD risks in PLWH. The discussion extends to critical future study areas related to vascular aging, CVD, and the efficacy of exercise interventions, with a call for more inclusive research that considers the diversity of the PLWH population.

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Cardiometabolic and vascular effects of treatment with a fixed-dose combination anti-retroviral drug containing nucleoside and non-nucleoside reverse transcriptase inhibitors (NRTI s and NNRTI s ) in adult rats

Cited by 4 publications

References 0 publications

Vascular endothelial dysfunction in the wake of HIV and ART

Vascular endothelial dysfunction in the wake of HIV and ART

Exploring the NRF2/HO-1 and NF-κB Pathways: Spirulina Nanoparticles as a Novel Approach to Combat Diabetic Nephropathy

Exercise to Prevent Accelerated Vascular Aging in People Living With HIV

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