Monastyrska Iryna, Klionsky Daniel J
Life Sciences Institute, and Department of Molecular, University of Michigan, Ann Arbor, MI 48109, USA.
Mol Aspects Med. 2006 Oct-Dec;27(5-6):483-94. doi: 10.1016/j.mam.2006.08.004. Epub 2006 Sep 14.
When cells are confronted with an insufficient supply of nutrients in their extracellular fluid, they may begin to cannibalize some of their internal proteins as well as whole organelles for reuse in the synthesis of new components. This process is termed autophagy and it involves the formation of a double-membrane structure within the cell, which encloses the material to be degraded into a vesicle called an autophagosome. The autophagosome subsequently fuses with a lysosome/vacuole whose hydrolytic enzymes degrade the sequestered organelle. Degradation of peroxisomes is a specific type of autophagy, which occurs in a selective manner and has been mostly studied in yeast. Recently, it was reported that a similar selective process of autophagy occurs in mammalian cells with proliferated peroxisomes. Here we discuss characteristics of the autophagy of peroxisomes in mammalian cells and present a comprehensive model of their likely mechanism of degradation on the basis of known and common elements from other systems.
当细胞在细胞外液中面临营养供应不足时,它们可能会开始分解自身的一些内部蛋白质以及整个细胞器,以便在新成分的合成中重新利用。这个过程被称为自噬,它涉及在细胞内形成一种双膜结构,该结构将待降解的物质包裹进一个称为自噬体的囊泡中。自噬体随后与溶酶体/液泡融合,其水解酶会降解被隔离的细胞器。过氧化物酶体的降解是一种特定类型的自噬,它以选择性方式发生,并且主要在酵母中得到研究。最近,有报道称在过氧化物酶体增殖的哺乳动物细胞中也发生了类似的选择性自噬过程。在此,我们讨论哺乳动物细胞中过氧化物酶体自噬的特征,并基于来自其他系统的已知和共同元素,提出一个关于其可能降解机制的综合模型。