Biologic effect and molecular regulation of vascular apoptosis in atherosclerosis.
Biologic effect and molecular regulation of vascular apoptosis in atherosclerosis.
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DOI：
10.1007/s11883-001-0066-z
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发表时间：
2001-05-01
影响因子：
5.8
通讯作者：
Geng, Y J
中科院分区：
文献类型：
--
作者：
Geng, Y J
细胞凋亡是一种遗传程序性细胞死亡，在动脉壁细胞结构的调节中起着关键作用。在动脉粥样硬化形成过程中，细胞凋亡失调可能导致动脉形态发生、管壁结构稳定性和代谢异常。许多生物生理生化因素，包括机械力、活性氧和氮、细胞因子、生长因子、氧化脂蛋白等都可能影响血管细胞凋亡。Fas/Fas配体/caspase死亡信号通路、Bcl-2蛋白家族/线粒体、肿瘤抑制基因p53和原癌基因c-myc可能在动脉粥样硬化病变中被激活并介导血管凋亡。这些凋亡调控基因的异常表达和功能障碍可减弱或加速血管细胞凋亡，影响斑块的完整性和稳定性。阐明细胞凋亡调控的分子机制，将有助于设计治疗动脉粥样硬化及其主要并发症急性血管综合征的新策略。
Apoptosis, a form of genetically programmed cell death, plays a key role in regulation of cellularity of the arterial wall. During atherogenesis, deregulated apoptosis may cause abnormalities of arterial morphogenesis, wall structural stability, and metabolisms. Many biophysiologic and biochemical factors, including mechanical forces, reactive oxygen and nitrogen species, cytokines, growth factors, oxidized lipoproteins, etc. may influence apoptosis of vascular cells. The Fas/Fas ligand/caspase death-signaling pathway, Bcl-2 protein family/mitochondria, the tumor suppressive gene p53, and the proto-oncogene c-myc may be activated in atherosclerotic lesions and mediate vascular apoptosis during the development of atherosclerosis. Abnormal expression and dysfunction of these apoptosis-regulating genes may attenuate or accelerate vascular cell apoptosis and affect the integrity and stability of plaques. Clarification of the molecular mechanism that regulates apoptosis may help design a new strategy for treatment of atherosclerosis and its major complication, the acute vascular syndromes.