Aging as a mitochondria-mediated atavistic program - Can aging be switched off?
Aging as a mitochondria-mediated atavistic program - Can aging be switched off?
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DOI：
10.1196/annals.1356.009
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Longo, VD
中科院分区：
文献类型：
--
作者：
Skulachev, VP;Longo, VD
程序性死亡现象已经在亚细胞(有丝分裂)、细胞(凋亡)和超细胞(集体凋亡)水平上被证明。在生物体层面上有许多自杀机制的例子(脱垂)。在酵母中，最近的研究表明，衰老细胞的死亡是程序化的。细胞程序性死亡的许多步骤在酵母和动物(包括哺乳动物)中是常见的。特别是，线粒体活性氧物种(ROS)的产生参与了自杀计划。高等动物的衰老伴随着线粒体ROS损伤的增加。或许，通过清除线粒体ROS来防止这种损伤，可能会减缓甚至关闭衰老程序。
Programmed death phenomena have been demonstrated on subcellular (mitoptosis), cellular (apoptosis), and supracellular (collective apoptosis) levels. There are numerous examples of suicide mechanisms at the organismal level (phenoptosis). In yeast, it was recently shown that the death of aging cells is programmed. Many of the steps of programmed cell death are shown to be common for yeast and animals, including mammals. In particular, generation of the mitochondrial reactive oxygen species (ROS) is involved in the suicide programs. Aging of higher animals is accompanied by an increase in damage induced by mitochondrial ROS. Perhaps prevention of such damage by scavenging of mitochondrial ROS might slow down or even switch off the aging programs.