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细胞自噬是哺乳动物细胞物质代谢的一种重要机制,细胞自噬异常将导致细胞功能异常甚至死亡。细胞自噬异常在卵巢早衰(POF)的发病中扮演着重要的角色,细胞自噬与细胞凋亡之间存在着许多分子联系,凋亡相关蛋白Bcl-2、Caspase与自噬相关蛋白Beclin-1互相作用,可以引起卵巢发育异常;凋亡蛋白Bim、Fas与自噬相关信号通路PTEN-PI3K及下游转录因子Fox O蛋白互相作用,可以导致卵巢卵泡激活异常;激素异常通过TGF-β/Smad3通路介导凋亡和自噬相关蛋白异常,导致卵泡闭锁,从而可以导致POF的发病。细胞自噬极有可能与细胞凋亡一起,是POF的主要发病机制。
Autophagy is an important mechanism of the metabolism of mammalian cell material. Abnormal cell autophagy will lead to cell dysfunction and even death. The abnormal autophagy plays an important role in the pathogenesis of POF. There are many molecular links between autophagy and apoptosis. The expression of Bcl-2, Caspase and autophagy-related protein Beclin- 1 interaction can cause ovarian dysplasia; apoptosis protein Bim, Fas and autophagy-related signaling pathway PTEN-PI3K and downstream transcription factor Fox O protein interaction, can lead to abnormal ovarian follicle activation; abnormal hormone through TGF-β / Smad3 Pathway-mediated apoptosis and autophagy-related protein abnormalities, leading to atresia follicles, which can lead to the incidence of POF. Autophagy is most likely associated with apoptosis, which is the main pathogenesis of POF.