De Caterina R, Lenzi S
Istituto di Fisiologia Clinica, CNR, Pisa.
G Ital Cardiol. 1998 Feb;28(2):158-67.
The existence of a causal relation between elevated cholesterol levels and atherosclerosis is now considered an established fact, while cellular and molecular mechanisms underlying this relationship begin only now to be unravelled. The first stage of atherosclerosis development is the fatty streak, a focal accumulation of blood-derived lipid-laden macrophages in the arterial intima. The endothelium, which plays a pivotal role in vascular homeostasis, undergoes major functional changes under the influence of "oxidized" and "minimally-modified"-LDL, able to promote "endothelial activation", with the expression of adhesion molecules and chemoattractants for monocytes. Endothelial activation seems to be the transducer of atherogenic signals in the first stages of development of atherosclerosis. LDL also play a further crucial role in the progression and the instabilization of the plaque, and in the pathogenesis of functional changes of vasomotor tone.
胆固醇水平升高与动脉粥样硬化之间存在因果关系，如今这已被视为既定事实，而这种关系背后的细胞和分子机制才刚刚开始被揭示。动脉粥样硬化发展的第一阶段是脂纹，即动脉内膜中源自血液的载脂巨噬细胞的局灶性聚集。在内皮功能的维持中起关键作用的内皮，在“氧化型”和“轻度修饰型”低密度脂蛋白（LDL）的影响下会发生重大功能变化，这些脂蛋白能够促进“内皮激活”，使内皮细胞表达黏附分子和单核细胞趋化因子。内皮激活似乎是动脉粥样硬化发展初期致动脉粥样硬化信号的传导介质。低密度脂蛋白在斑块的进展、不稳定以及血管舒缩张力功能变化的发病机制中也起着进一步的关键作用。
