Role of mitochondria in neuronal apoptosis
Role of mitochondria in neuronal apoptosis
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DOI：
10.1159/000017460
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发表时间：
2000-09-01
影响因子：
2.9
通讯作者：
Orrenius, S
中科院分区：
文献类型：
--
作者：
Gorman, AM;Ceccatelli, S;Orrenius, S
细胞凋亡是细胞死亡的一种受控形式，参与神经元细胞在发育、神经退行性疾病和接触神经毒剂过程中的死亡。近年来，线粒体已成为控制细胞凋亡的关键，它们含有许多凋亡分子，在细胞凋亡开始时释放到细胞质中，包括细胞色素c、凋亡诱导因子和各种半胱天冬酶，线粒体还在细胞内Ca2+调节中发挥重要作用，这对兴奋性毒性至关重要 神经变性。线粒体能量（ATP）产生的改变（由于缺氧或编码电子传递链线粒体蛋白的基因突变）可以诱导神经元细胞凋亡或增加其对细胞凋亡的敏感性。版权所有 (C) 2000 S. Karger AG，巴塞尔。
Apoptosis is a controlled form of cell death that participates in the demise of neuronal cells during development, neurodegenerative disorders and exposure to neurotoxic agents. In recent years, the mitochondria have emerged as being pivotal in controlling apoptosis, They house a number of apoptogenic molecules that are released into the cytoplasm at the onset of apoptosis, These include cytochrome c, apoptosis-inducing factor and various caspases, Mitochondria also play an important role in intracellular Ca2+ regulation, which is crucial to excitotoxic neurodegeneration. Alterations in energy (ATP) production by mitochondria (due to hypoxia or mutations in genes encoding mitochondrial proteins of the electron transport chain) can induce apoptosis in neurons or increase their sensitivity to apoptosis. Copyright (C) 2000 S. Karger AG, Basel.