Libby P, Aikawa M, Jain M K
Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Handb Exp Pharmacol. 2006(176 Pt 2):285-306. doi: 10.1007/3-540-36028-x_9.
Atherosclerosis depends critically on altered behavior of the intrinsic cells of the artery wall, the endothelial cells and smooth muscle cells, and inflammatory leukocytes that join them in the arterial intima during the atherogenic process. The homeostatic properties of the normal endothelium contribute importantly to maintenance of aspects of arterial health including the appropriate regulation of blood flow, a basal anti-inflammatory state, promotion of fibrinolysis while opposing blood coagulation, and control of the balance of cellular proliferation and death. Alterations in these endothelial homeostatic mechanisms contribute critically to atherogenesis, the progression of this disease, and ist complications. Recent advances have highlighted novel molecular mechanisms that regulate the atheroprotective functions of normal endothelial cells that go awry during atherogenesis. Therapeutic strategies that alter the course of atherosclerosis may act by combating endothelial dysfunction.
动脉粥样硬化严重依赖于动脉壁固有细胞（内皮细胞和平滑肌细胞）以及在动脉粥样硬化形成过程中进入动脉内膜的炎性白细胞行为的改变。正常内皮的稳态特性对维持动脉健康的多个方面起着重要作用，包括对血流的适当调节、基础抗炎状态、促进纤维蛋白溶解同时抑制血液凝固，以及控制细胞增殖与死亡的平衡。这些内皮稳态机制的改变对动脉粥样硬化的发生、疾病进展及其并发症起着关键作用。最近的进展突出了调节正常内皮细胞抗动脉粥样硬化功能的新分子机制，这些机制在动脉粥样硬化形成过程中出现异常。改变动脉粥样硬化进程的治疗策略可能通过对抗内皮功能障碍来发挥作用。
