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[细胞凋亡在动脉粥样硬化发病机制中的作用]

[Role of apoptosis in the pathogenesis of atherosclerosis].

作者信息

Bits' Iu V, Dosenko V Ie, Medvedev V V

机构信息

O.O. Bogomolets National Medical University, Ukrainian Ministry of Public Health, Kyiv, Ukraine.

出版信息

Fiziol Zh (1994). 2000;46(5):83-93.

PMID:11269859
Abstract

The recent information about importance of programmed cell death in the development of atherosclerosis was reviewed. It was emphasized, that intensiveness of apoptosis was various for smooth muscle cells, macrophages, endothelial cells, lymphocytes, and changed during the development of such a multistage process as atherosclerosis. Is was proved, that exactly apoptosis gave specific features to the atherosclerotic process. The agents inducing atherosclerosis (modified lipoprotein, mechanical influences, viruses, bacterial toxins, etc.), have insufficient for initiation of necrosis. The damage to vascular wall in atherosclerosis is characterized not by intensive influence of pathogenic factors, but rather constant chronic influence of the agents of moderate power. Therefore, it is just apoptosis that makes up the critical mechanism of the reactive-regeneration answer of vascular wall structures to an injure. Evolutionally, the apoptic way of the development of answer to an injure appears to be more rational, as for as it results in minimal losses of cells due to both secondary alteration and maintenance of fast restoration of the primary cellular architecture of injured tissues at the expense of the natural mechanisms of regulation of apoptosis and proliferation. In the certain situation, these positive aspects of apoptosis make up a basis for the development of a pathology--failures in the program of apoptosis result in chronic proliferative-degenerative processes, that is in atherosclerosis.

摘要

综述了近期关于程序性细胞死亡在动脉粥样硬化发展过程中的重要性的信息。强调指出,凋亡强度在平滑肌细胞、巨噬细胞、内皮细胞、淋巴细胞中各不相同,并且在动脉粥样硬化这样一个多阶段过程的发展过程中会发生变化。已证实,正是凋亡赋予了动脉粥样硬化过程特定的特征。诱导动脉粥样硬化的因素(修饰的脂蛋白、机械影响、病毒、细菌毒素等)不足以引发坏死。动脉粥样硬化中血管壁的损伤并非以致病因素的强烈影响为特征,而是以中等强度因素的持续慢性影响为特征。因此,正是凋亡构成了血管壁结构对损伤的反应性再生应答的关键机制。从进化角度来看,损伤应答的凋亡发展方式似乎更为合理,因为它由于继发性改变以及以凋亡和增殖的自然调节机制为代价维持受损组织原始细胞结构的快速恢复,从而导致细胞损失最小。在某些情况下,凋亡的这些积极方面构成了一种病理学发展的基础——凋亡程序的失败会导致慢性增殖 - 退行性过程,即动脉粥样硬化。

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