McGrath L T, Elliott R J
Division of Biochemistry, School of Biology and Biochemistry, Queen's University of Belfast, Northern Ireland, U.K.
Atherosclerosis. 1991 Apr;87(2-3):211-20. doi: 10.1016/0021-9150(91)90023-v.
The smooth muscle cell invasion and macrophage stimulation within the intima during prolonged exposure to high blood levels of cholesterol esters contribute to increased production of connective tissue matrix. The thickened intima in turn immobilising more LDL derived lipid from the plasma. With damage to the internal elastic lamellae, from essential hypertension, the absorbed lipid can move down a concentration gradient into the medial tissue. This model was supported by our laboratory finding of a lipid gradient across the aorta wall. The gradient commenced shortly after completion of body growth, when the transmedial gradient became detectable. The slope of the gradient progressively increased during ageing. Association of the lipid medial gradient with the degree of atherosclerotic involvement suggested that the gradient influenced the development of intimal lesions. Accumulation of lipid within the medial tissue may then reduce the inward lipid transfer rate from the intima, promoting increased intimal retention and cause the formation of atherosclerotic plaques from the fat saturated intima.
长时间暴露于高血胆固醇酯水平会导致内膜中的平滑肌细胞浸润和巨噬细胞激活，进而促进结缔组织基质生成增加。增厚的内膜反过来又会固定更多来自血浆的低密度脂蛋白衍生脂质。由于原发性高血压导致内弹性膜受损，吸收的脂质可沿浓度梯度进入中膜组织。我们实验室在主动脉壁上发现的脂质梯度支持了这一模型。这种梯度在身体生长完成后不久就开始出现，此时跨中膜梯度变得可检测到。在衰老过程中，梯度的斜率逐渐增加。脂质中膜梯度与动脉粥样硬化累及程度的关联表明，这种梯度影响内膜病变的发展。然后，中膜组织内的脂质积累可能会降低脂质从内膜向内的转运速率，促进内膜脂质潴留增加，并导致脂肪饱和的内膜形成动脉粥样硬化斑块。
