Beaudeux J L, Jacob N, Giral P, Foglietti M J, Bruckert E
Service de Biochimie C, Fédération de Biochimie, Groupe Hospitalier Pitié-Salpêtriére, AP-HP, 47-83, boulevard de l'Hôpital, 75651 Paris Cedex 13, France.
Ann Med Interne (Paris). 2001 Apr;152(3):169-79.
Recent research indicates that both inflammation and infection of coronary arteries are intimately involved in the development and the progression of atherosclerosis. Pathophysiological mechanisms of formation of the atheromatous plaque are complex, resulting from the activation of endothelial cells, monocytes and foam cells, and smooth muscle cells. Numerous molecules are involved in these mechanisms, including adhesion molecules, pro-inflammatory and anti-inflammatory cytokines, chemokines, extracellular matrix remodelling enzymes, coagulation and fibrinolysis factors and infectious agents. Studies have suggested a potential role for these molecules as markers of the development of coronary artery disease and of adverse cardiac-related outcomes in patients with known coronary artery syndromes, in combination with independent risk factors such as homocysteine. This review presents recent data that could contribute to use of these markers for the diagnosis and the evolution of atherosclerosis. in clinical practice.
近期研究表明,冠状动脉的炎症和感染与动脉粥样硬化的发生和发展密切相关。动脉粥样斑块形成的病理生理机制复杂,是由内皮细胞、单核细胞、泡沫细胞和平滑肌细胞的激活所致。许多分子参与这些机制,包括黏附分子、促炎和抗炎细胞因子、趋化因子、细胞外基质重塑酶、凝血和纤维蛋白溶解因子以及感染因子。研究表明,这些分子与同型半胱氨酸等独立危险因素相结合,可能作为已知冠状动脉综合征患者冠状动脉疾病发展及不良心脏相关结局的标志物。本综述介绍了近期的数据,这些数据可能有助于在临床实践中利用这些标志物来诊断和评估动脉粥样硬化的进展。