scholarly journals Epicardial Adipose Tissue as a Source of Nuclear Factor-κB and c-Jun N-Terminal Kinase Mediated Inflammation in Patients with Coronary Artery Disease

2009 ◽  
Vol 94 (1) ◽  
pp. 261-267 ◽  
Author(s):  
A. R. Baker ◽  
A. L. Harte ◽  
N. Howell ◽  
D. C. Pritlove ◽  
A. M. Ranasinghe ◽  
...  

Abstract Context: Visceral adipose tissue (AT) is known to confer a significantly higher risk of type 2 diabetes and cardiovascular disease. Epicardial AT has been shown to be related to cardiovascular disease and myocardial function through unidentified mechanisms. Epicardial AT expresses an inflammatory profile of proteins; however, the mechanisms responsible are yet to be elucidated. Objectives: The objectives of the study were to: 1) examine key mediators of the nuclear factor-κB (NFκB) and c-Jun N-terminal kinase (JNK) pathways in paired epicardial and gluteofemoral (thigh) AT from coronary artery disease (CAD) and control patients and 2) investigate circulating endotoxin levels in CAD and control subjects. Design: Serums and AT biopsies (epicardial and thigh) were obtained from CAD (n = 16) and non-CAD (n = 18) patients. Inflammation was assessed in tissue and serum samples through Western blot, real-time PCR, ELISAs, and activity studies. Results: Western blotting showed epicardial AT had significantly higher NFκB, inhibitory-κB kinase (IKK)-γ, IKKβ, and JNK-1 and -2 compared with thigh AT. Epicardial mRNA data showed strong correlations between CD-68 and toll-like receptor-2, toll-like receptor-4, and TNF-α. Circulating endotoxin was elevated in patients with CAD compared with matched controls [CAD: 6.80 ± 0.28 endotoxin unit(EU)/ml vs. controls: 5.52 ± 0.57 EU/ml; P<0.05]. Conclusion: Epicardial AT from patients with CAD shows increased NFκB, IKKβ, and JNK expression compared with both CAD thigh AT and non-CAD epicardial AT, suggesting a depot-specific as well as a disease-linked response to inflammation. These studies implicate both NFκB and JNK pathways in the inflammatory profile of epicardial AT and highlight the role of the macrophage in the inflammation within this tissue.

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  

Author(s):  
Rutao Wang ◽  
Scot Garg ◽  
Chao Gao ◽  
Hideyuki Kawashima ◽  
Masafumi Ono ◽  
...  

Abstract Aims To investigate the impact of established cardiovascular disease (CVD) on 10-year all-cause death following coronary revascularization in patients with complex coronary artery disease (CAD). Methods The SYNTAXES study assessed vital status out to 10 years of patients with complex CAD enrolled in the SYNTAX trial. The relative efficacy of PCI versus CABG in terms of 10-year all-cause death was assessed according to co-existing CVD. Results Established CVD status was recorded in 1771 (98.3%) patients, of whom 827 (46.7%) had established CVD. Compared to those without CVD, patients with CVD had a significantly higher risk of 10-year all-cause death (31.4% vs. 21.7%; adjusted HR: 1.40; 95% CI 1.08–1.80, p = 0.010). In patients with CVD, PCI had a non-significant numerically higher risk of 10-year all-cause death compared with CABG (35.9% vs. 27.2%; adjusted HR: 1.14; 95% CI 0.83–1.58, p = 0.412). The relative treatment effects of PCI versus CABG on 10-year all-cause death in patients with complex CAD were similar irrespective of the presence of CVD (p-interaction = 0.986). Only those patients with CVD in ≥ 2 territories had a higher risk of 10-year all-cause death (adjusted HR: 2.99, 95% CI 2.11–4.23, p < 0.001) compared to those without CVD. Conclusions The presence of CVD involving more than one territory was associated with a significantly increased risk of 10-year all-cause death, which was non-significantly higher in complex CAD patients treated with PCI compared with CABG. Acceptable long-term outcomes were observed, suggesting that patients with established CVD should not be precluded from undergoing invasive angiography or revascularization. Trial registration SYNTAX: ClinicalTrials.gov reference: NCT00114972. SYNTAX Extended Survival: ClinicalTrials.gov reference: NCT03417050. Graphic abstract


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Sabet ◽  
S Elkaffas ◽  
S.W.G Bakhoum ◽  
H Kandil

Abstract Introduction Smoking and obesity are recognized as important modifiable risk factors for coronary artery disease (CAD). However, the general perception that smoking protects against obesity is a common reason for starting, and/or not quitting smoking. Purpose To detect the quantity, quality and relative distribution of subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) estimated by abdominal computed tomography in smokers versus non- smokers. Methods The abdominal muscular wall was traced manually to calculate SAT and VAT areas (cm2) (outside and inside abdominal muscular wall respectively) as well as SAT density [Hounsfield units (HU)] at L4-L5 in 409 consecutive patients referred for evaluation of chest pain by multi-slice computed tomography coronary angiography (MSCT-CA). Results 26% of the studied patients (n=107) were current smokers, while the remaining 74% (n=302) never smoked. Coronary artery atherosclerosis was more prevalent in smokers compared to non-smokers (64.5% vs 55.0%; p=0.09). Smokers had statistically significantly lower body mass index (BMI) (31.2±4.3 vs. 32.5±4.7 kg/m2; p=0.015), hip circumference (HC) (98.6±22.5 vs. 103.9±20.9 cm; p=0.031), total fat area (441.62±166.34 vs. 517.95±169.51cm2; p&lt;0.001), and SAT area (313.07±125.54 vs. 390.93±143.28 cm2; p&lt;0.001) as compared to non-smokers. However, smokers had statistically significantly greater waist-to-hip ratio (0.98±0.08 vs. 0.96±0.08; p=0.010), VAT/SAT area ratio (0.41±0.23 vs. 0.35±0.20; p=0.013), and denser SAT depot (−98.91±7.71 vs. −102.08±6.44 HU; p&lt;0.001). Conclusion Smoking contributes to CAD and to the pathogenic redistribution of body fat towards VAT, through limiting SAT potential to expand. Funding Acknowledgement Type of funding source: None


Immunobiology ◽  
2012 ◽  
Vol 217 (5) ◽  
pp. 533-539 ◽  
Author(s):  
Mamoru Satoh ◽  
Tsuyoshi Tabuchi ◽  
Yoshitaka Minami ◽  
Yuji Takahashi ◽  
Tomonori Itoh ◽  
...  

Author(s):  
Elifcan Gezer ◽  
Mehtap Cevik ◽  
Cansu Selcan Akdeniz ◽  
Ismail Polat Canbolat ◽  
Selen Yurdakul ◽  
...  

Objective: Coronary artery disease (CAD) is the one of the leading cause of morbidity and mortality worldwide and statins are frequently prescribed in the treatment of CAD to help lower blood cholesterol levels. Since the main enzyme involved in the metabolism of statins is CYP3A4, we aimed to investigate the effect of CYP3A4 * 1B genotypes on plasma lipid profile in Turkish cardiovascular disease subject with and without obesity taking statin. Materials and Methods: The study group consisted of 85 cardiovascular disease patients who were prescribed statins and had routine biochemical analysis data. Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) assay were performed for genotyping of CYP3A4 *1B (rs2740574) polymorphism. Results: Genotype distribution of CYP3A4 *1B polymorphism was found for homozygous wild (AA) and homozygous polymorphic (GG) genotypes as 94.1% and 5.9% respectively. We did not detect patients with heterozygous genotype in our study group. We found that the mean LDL-c, TG and TC levels were higher in patients with CYP3A4 *1B GG compared to AA genotype. The frequency of CYP3A4 *1B GG genotype frequency (9.5%) was detected higher in the obese patients compared to the non-obese patients (7.7%) (χ2=0.037, p=0.85). Conclusions: Our results demonstrate that CYP3A4 *1B homozygous polymorphic genotype distribution tend to be higher in obese patients compared to non- obese patients with cardiovascular disease which may point *1B allele to have a slight effect on serum lipids during statin therapy. Additional studies with higher samples are needed for evaluating the role of CYP3A4 *1B on lipids in patients under statin therapy.


2015 ◽  
Vol 78 (3) ◽  
Author(s):  
Teresa Strisciuglio ◽  
Gennaro Galasso ◽  
Dario Leosco ◽  
Roberta De Rosa ◽  
Giuseppe Di Gioia ◽  
...  

Adipose tissue, besides being an important energetic storage, is also a source of cytokines and hormones which act in a paracrine, autocrine and especially endocrine manner, influencing the cardiometabolic axis. Adipokines are a group of mediators with pleiotropic function, that are involved in many physiological processes, so that a disregulation in their secretion can lead to multiple pathological conditions. In this review our aim was to clarify the role of adipokines in the pathogenesis of atherosclerosis, especially in coronary artery disease, and based on current scientific evidence, to analyze the therapeutic and behavioral strategies that are so far available.


2014 ◽  
Vol 55 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Se-Hong Kim ◽  
Ju-Hye Chung ◽  
Beom-June Kwon ◽  
Sang-Wook Song ◽  
Whan-Seok Choi

Sign in / Sign up

Export Citation Format

Share Document