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动脉粥样硬化与斑块并发症的病理生物学

Pathobiology of atherosclerosis and plaque complications.

作者信息

Dzau V J

机构信息

Division of Cardiovascular Medicine, Falk Cardiovascular Research Center, Stanford University School of Medicine, CA 94305-5246.

出版信息

Am Heart J. 1994 Dec;128(6 Pt 2):1300-4. doi: 10.1016/0002-8703(94)90251-8.

Abstract

To understand the process of atherosclerosis, the homeostatic and protective functions of the endothelium must be considered. The endothelium serves as the interface between blood flow and the vascular tissues. It normally regulates vascular tone and structure through the release of vasoactive substances and maintenance of a nonthrombogenic surface. Endothelial dysfunction, which results from biochemical and hemodynamic stresses associated with cardiovascular risk factors, causes an imbalance in the expression of vasodilating and vasoconstricting substances, as well as excess production of chemoattractant molecules and growth factors. Endothelial dysfunction in the presence of elevated cholesterol levels fosters the development of fatty streaks, which represent the early stage of atherosclerotic plaque. The unstable progression of atherosclerosis can be interrupted and even reversed in both animals and humans, although the exact clinical correlates of progression and regression are not fully understood.

摘要

为了解动脉粥样硬化的过程,必须考虑内皮的稳态和保护功能。内皮作为血流与血管组织之间的界面。它通常通过释放血管活性物质和维持非血栓形成表面来调节血管张力和结构。内皮功能障碍由与心血管危险因素相关的生化和血流动力学应激引起,导致血管舒张和收缩物质表达失衡,以及趋化分子和生长因子的过量产生。在胆固醇水平升高的情况下,内皮功能障碍促进脂肪条纹的发展,脂肪条纹代表动脉粥样硬化斑块的早期阶段。动脉粥样硬化的不稳定进展在动物和人类中都可以被阻断甚至逆转,尽管进展和逆转的确切临床关联尚未完全了解。

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