Modulation of endothelial cell apoptosis: mechanisms and pathophysiological roles.
Modulation of endothelial cell apoptosis: mechanisms and pathophysiological roles.
复制标题
DOI：
10.5551/jat1994.3.75
复制
发表时间：
1996
影响因子：
4.4
通讯作者：
A. Karsan;J. Harlan
中科院分区：
文献类型：
--
作者：
A. Karsan;J. Harlan
细胞凋亡是细胞死亡的一种模式，其中内在细胞机制参与细胞的死亡。内皮细胞凋亡的调节可能在动脉粥样硬化、血管新生、血管重塑等病理生理状态中发挥作用。细胞死亡的控制由死亡途径的活化状态以及抗凋亡蛋白的水平介导。许多（如果不是全部）细胞凋亡触发物的最终共同途径涉及半胱氨酸蛋白酶的活化。相反，Bcl 2家族似乎在防止细胞凋亡中起主要作用。这些机制在调节内皮细胞凋亡在各种条件下的作用进行了讨论。
Apoptosis is a mode of cell death in which intrinsic cellular mechanisms participate in the demise of the cell. The modulation of endothelial apoptosis may play a role in atherosclerosis, angiogenesis, vascular remodeling and other pathophysiological states. Control of cell death is mediated by the state of activation of a death pathway as well as by the levels of anti apoptotic proteins. The final common pathway of many, if not all, triggers of apoptosis involves activation of cysteine proteases. The Bcl 2 family, in contrast, appears to play a major role in protection against apoptosis. The role of these mechanisms in modulating endothelial cell apoptosis under various conditions is discussed.