Common community infections and the risk for coronary artery disease and acute myocardial infarction: Evidence for chronic over-expression of tumor necrosis factor alpha and vascular cells adhesion molecule-1

Nikolopoulou, Aggeliki; Tousoulis, Dimitris; Antoniades, Charalambos; Petroheilou, Katerina; Vasiliadou, Carmen; Papageorgiou, Nikolaos S.; Koniari, Katerina; Stefanadi, Elli; Latsios, George; Siasos, Gerasimos; Stefanadis, Christodoulos

doi:10.1016/j.ijcard.2007.08.052

Cited by 26 publications

(18 citation statements)

References 15 publications

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“…A study in northwest of Iran revealed more than 98% seropositivity for CMV in a group of healthy blood donors (34). Also, the results of the research by Nikolopoulou et al indicated the rate of anti-CMV IgG to be 95.5% among the patients with angiographically-documented stable CAD (35), which is similar to our findings in the CAD group. Alavi et al also performed a study in southern Iran and reported a high rate of anti-CMV IgG seropositivity in patients with CAD as well as in controls (93% of the patients with unstable angina and 96.7% of the controls) (11).…”

Section: Discussionsupporting

confidence: 92%

Cytomegalovirus Infection and Coronary Artery Disease: A Single-Center Serological Study in Northwestern Iran

Khameneh¹,

Rostamzadeh²,

Nemati³

et al. 2016

Int Cardiovasc Res J

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Section: Discussionsupporting

confidence: 92%

Cytomegalovirus Infection and Coronary Artery Disease: A Single-Center Serological Study in Northwestern Iran

Khameneh¹,

Rostamzadeh²,

Nemati³

et al. 2016

Int Cardiovasc Res J

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“…Our data can explain the PTX-dependent reduction of sVCAM-1, which is a surrogate marker for endothelial VCAM-1 production, in HIV-positive individuals. 36,37 To test our hypothesis that cooperation between HIV and inflammatory cytokines may be a mechanism leading to HIV-associated cardiovascular disease, we assessed for a potential HIV and TNF-a synergy in HCAECs. In this study we focused on the effect of HIV proteins on VCAM-1 since it was upregulated in the in vivo trials and is specific for endothelial cells, whereas other TNFregulated inflammatory proteins, such as ICAM-1 and IL-6, are also expressed in other cell types.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline Reduces Tumor Necrosis Factor-α and HIV-Induced Vascular Endothelial Activation

Green

Kim

Gupta

et al. 2012

AIDS Research and Human Retroviruses

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Untreated HIV infection is associated with endothelial dysfunction and subsequent cardiovascular disease, likely due to both direct effects of the virus and to indirect effects of systemic inflammation on the vasculature. We have recently shown that treatment with the antiinflammatory agent pentoxifylline (PTX) improved in vivo endothelial function and reduced circulating levels of the inflammatory markers vascular cell adhesion molecule-1 (VCAM-1) and interferon-gamma-induced protein (IP-10) in HIV-infected patients. To delineate the mechanisms underlying this therapeutic effect, we tested whether clinically relevant concentrations of PTX suppress VCAM-1 or IP-10 release in cultivated human lung microvascular endothelial cells. Indeed, we found that tumor necrosis factor (TNF)-a-induced VCAM-1 was reduced with concentrations of PTX in the low nanomolar range, comparable to plasma levels in PTX-treated groups. We also investigated the effect of HIV proteins and found that HIV transactivator of transcription (HIV-Tat) and HIV-envelope-derived recombinant gp120 enhanced TNF-a-induced VCAM-1 gene expression in lung microvascular and coronary macrovascular endothelial cells, respectively. In addition, PTX and a NF-jB-specific inhibitor reduced this enhanced VCAM-1 gene induction in microvascular and macrovascular endothelial cells. These results provide novel insights in how the antiinflammatory agent PTX can directly reduce HIV-associated proinflammatory endothelial activation, which may underlie vascular dysfunction and coronary vascular diseases.

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“…In healthy subjects, increased circulating plasma levels of TNFa predict the risk for cardiovascular diseases [259][260][261], especially in men [262]. An increased circulating TNFa concentration correlates to the impairment in cardiac function [263,264] and is an independent predictor of reduced event-free survival [261], the development of heart failure in asymptomatic patients without prior MI [265,266], and mortality in patients with advanced heart failure [267][268][269].…”

Section: Tnfa As a Biomarker Of Heart Failurementioning

confidence: 99%

“…An increased circulating TNFa concentration correlates to the impairment in cardiac function [263,264] and is an independent predictor of reduced event-free survival [261], the development of heart failure in asymptomatic patients without prior MI [265,266], and mortality in patients with advanced heart failure [267][268][269]. In Japanese patients with idiopathic dilated cardiomyopathy, the polymorphism of the TNFA2 gene was not associated with the clinical course of the disease [81], and this finding was confirmed in a metaanalysis of genetic variations associated with ischemic heart failure [82].…”

Section: Tnfa As a Biomarker Of Heart Failurementioning

confidence: 99%

TNFα in myocardial ischemia/reperfusion, remodeling and heart failure

2010

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TNFα is crucially involved in the pathogenesis and progression of myocardial ischemia/reperfusion injury and heart failure. The formation and release of TNFα and its downstream signal transduction cascade following activation of its two receptor subtypes are characterized. Myocardial TNFα and TNF receptor activation have an ambivalent role in myocardial ischemia/reperfusion injury and protection from it. Excessive TNFα expression and subsequent cardiomyocyte TNF receptor type 1 stimulation induce contractile dysfunction, hypertrophy, fibrosis and cell death, while a lower TNFα concentration and subsequent cardiomyocyte TNF receptor type 2 stimulation are protective. Apart from its concentration and receptor subtype, the myocardial action of TNFα depends on the duration of its exposure and its localization. While detrimental during sustained ischemia, TNFα contributes to ischemic preconditioning protection, no matter whether it is the first, second or third window of protection, and both TNF receptors are involved in the protective signal transduction cascade. Finally, the available clinical attempts to antagonize TNFα in cardiovascular disease, notably heart failure, are critically discussed.

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Common community infections and the risk for coronary artery disease and acute myocardial infarction: Evidence for chronic over-expression of tumor necrosis factor alpha and vascular cells adhesion molecule-1

Cited by 26 publications

References 15 publications

Cytomegalovirus Infection and Coronary Artery Disease: A Single-Center Serological Study in Northwestern Iran

Cytomegalovirus Infection and Coronary Artery Disease: A Single-Center Serological Study in Northwestern Iran

Pentoxifylline Reduces Tumor Necrosis Factor-α and HIV-Induced Vascular Endothelial Activation

TNFα in myocardial ischemia/reperfusion, remodeling and heart failure

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