1] Institut national de la santé et de la recherche médicale (INSERM), U1138, F-94805 Villejuif, France. [2] Université Paris Descartes/Paris V, Sorbonne Paris Cité, F-75006 Paris, France.
Department of Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.
Nat Rev Mol Cell Biol. 2014 Feb;15(2):81-94. doi: 10.1038/nrm3735. Epub 2014 Jan 8.
Autophagy and apoptosis control the turnover of organelles and proteins within cells, and of cells within organisms, respectively, and many stress pathways sequentially elicit autophagy, and apoptosis within the same cell. Generally autophagy blocks the induction of apoptosis, and apoptosis-associated caspase activation shuts off the autophagic process. However, in special cases, autophagy or autophagy-relevant proteins may help to induce apoptosis or necrosis, and autophagy has been shown to degrade the cytoplasm excessively, leading to 'autophagic cell death'. The dialogue between autophagy and cell death pathways influences the normal clearance of dying cells, as well as immune recognition of dead cell antigens. Therefore, the disruption of the relationship between autophagy and apoptosis has important pathophysiological consequences.
自噬和细胞凋亡分别控制着细胞内细胞器和蛋白质以及生物体内细胞的更新,许多应激途径会在同一细胞中依次引发自噬和细胞凋亡。一般来说,自噬会阻止细胞凋亡的诱导,而凋亡相关的半胱氨酸天冬氨酸蛋白酶的激活会终止自噬过程。然而,在特殊情况下,自噬或自噬相关蛋白可能有助于诱导细胞凋亡或坏死,并且自噬已被证明会过度降解细胞质,导致“自噬性细胞死亡”。自噬和细胞死亡途径之间的对话会影响到死亡细胞的正常清除以及对死亡细胞抗原的免疫识别。因此,自噬和细胞凋亡之间关系的破坏会产生重要的病理生理后果。