Apoptosis signaling pathways in lung diseases.
Apoptosis signaling pathways in lung diseases.
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DOI：
10.2174/1573406053402497
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
K. Kuwano;M. Yoshimi;T. Maeyama;N. Hamada;M. Yamada;Y. Nakanishi
中科院分区：
文献类型：
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作者：
K. Kuwano;M. Yoshimi;T. Maeyama;N. Hamada;M. Yamada;Y. Nakanishi
细胞凋亡在肺部疾病的病理生理过程中起重要作用的证据已经积累。细胞凋亡信号传导经典地由两个主要途径组成。一个是从死亡受体连接到半胱天冬酶级联激活和细胞死亡的直接途径。死亡受体连接通过衔接蛋白FADD触发半胱天冬酶-8的前体形式向死亡诱导复合物的募集，这导致半胱天冬酶-8活化。由刺激物如药物、辐射、感染因子和活性氧物质触发的另一途径在线粒体中启动。细胞色素c从线粒体释放到胞质溶胶后，与Apaf 1和ATP结合，然后激活caspase-9。近年来，内质网也被证明是执行细胞凋亡的细胞器。进一步了解细胞凋亡的分子机制及其通过新型药物的调节可能会导致对肺部疾病的有效策略的发展。我们概述了细胞凋亡的信号通路，并讨论了细胞凋亡在各种肺部疾病的病理生理学的参与。
Evidence that apoptosis plays an important role in the pathophysiology of lung diseases has been accumulated. Apoptosis signaling is classically composed of two principle pathways. One is a direct pathway from death receptor ligation to caspase cascade activation and cell death. Death receptor ligation triggers recruitment of the precursor form of caspase-8 to a death-inducing complex, through the adaptor protein FADD, which leads to caspase-8 activation. The other pathway triggered by stimuli such as drugs, radiation, infectious agents and reactive oxygen species is initiated in mitochondria. After cytochrome c is released into the cytosol from the mitochondria, it binds to Apaf1 and ATP, which then activate caspase-9. Recently, endoplasmic reticulum has also been shown to be the organelle to execute apoptosis. Further understanding of molecular mechanisms of apoptosis and its regulation by novel drugs may lead to the development of effective strategies against lung diseases. We overview the signaling pathways of apoptosis and discuss the involvement of apoptosis in the pathophysiology of various lung diseases.