DOI 10.1111/j.1365-2265.2006.02448.x
Tissue levels of adiponectin, tumour necrosis factor-alpha, soluble intercellular adhesion molecule-1 and heart-type fatty acid-binding protein in human coronary atherosclerotic plaques.
Аннотация
BACKGROUND
There is little information available about any link between the levels of adiponectin, intercellular adhesion molecule-1 (ICAM-1), tumour necrosis factor-alpha (TNF-alpha) and heart-type fatty acid-binding protein (H-FABP) in coronary atherosclerotic plaque specimens.
AIM: To analyse tissue levels of adiponectin, ICAM-1, TNF-alpha and H-FABP in the plaques obtained from coronary artery bypass grafting (CABG) and to evaluate whether there is any relationship between these variables and other characteristics.
PATIENTS AND
METHODS
Coronary artery specimens from 37 consecutive patients (28 men and nine women) at time of CABG procedure and preprocedural blood samples were obtained. Tissue concentrations of adiponectin, ICAM-1, TNF-alpha and H-FABP in the atherosclerotic plaques were measured.
RESULTS
Blood glucose and tissue levels of TNF-alpha and ICAM-1 were negatively correlated with tissue levels of adiponectin, whereas TNF-alpha was positively correlated with ICAM-1 in atherosclerotic plaques. In addition, there was a positive correlation between blood glucose and tissue levels of both TNF-alpha and ICAM-1. TNF-alpha and ICAM-1 levels in atherosclerotic plaques appear to progressively increase whereas adiponectin levels progressively decrease with smoking status. Atherosclerotic tissue levels of these substances are also altered in diabetes.
CONCLUSIONS
The data are in accord with those in prior publications on the detection and quantification of various inflammatory cytokines in atherosclerotic plaques. Our results indicate that diabetic state and smoking, in addition to other physiopathological mechanisms, may create a chronic inflammatory situation in the atherosclerotic process.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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