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缺氧和复氧过程中线粒体游离钙的调节:与细胞损伤的关系

Mitochondrial free calcium regulation in hypoxia and reoxygenation: relation to cellular injury.

作者信息

Silverman H S

机构信息

Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland.

出版信息

Basic Res Cardiol. 1993 Sep-Oct;88(5):483-94. doi: 10.1007/BF00795414.

Abstract

The role of mitochondria in myocardial ischemic and hypoxic injury is discussed. Increases in mitochondrial Ca content and ionized Ca2+ concentration are observed during and after ischemic and hypoxic exposure and have traditionally been considered to impair mitochondrial function. New data are discussed in which it is shown that increases in mitochondrial [Ca2+] do not necessarily reflect irreversible myocyte injury. Further, it is shown that irreversible cellular injury may occur in hypoxic myocytes in association with increases in mitochondrial [Ca2+] that would ordinarily be considered to fall within a physiologic range. The significance of these observations is considered in context with observations relating to the assessment of post-hypoxic mitochondrial function.

摘要

本文讨论了线粒体在心肌缺血缺氧损伤中的作用。在缺血缺氧暴露期间及之后,观察到线粒体钙含量和游离钙离子浓度增加,传统上认为这会损害线粒体功能。文中讨论了新的数据,这些数据表明线粒体[Ca2+]的增加不一定反映不可逆的心肌细胞损伤。此外,研究表明,在缺氧心肌细胞中,与线粒体[Ca2+]增加相关的不可逆细胞损伤可能会发生,而这种增加通常被认为处于生理范围内。结合与缺氧后线粒体功能评估相关的观察结果,对这些观察结果的意义进行了探讨。

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