缺氧对自噬双重作用调节的研究进展  

Recent advances in the regulation of hypoxia on autophagy

作　　者：徐涛[1] 张杰[1] 

机构地区：[1]武汉大学人民医院泌尿外科,430060

出　　处：《疑难病杂志》2017年第7期750-754,共5页Chinese Journal of Difficult and Complicated Cases

基　　金：国家自然科学基金资助项目(81470923)

摘　　要：自噬是维持细胞内环境稳定的一个重要机制,与缺氧引起的细胞凋亡密切相关。一般来说,自噬能够阻碍细胞凋亡的诱导,抑制细胞凋亡相关蛋白酶的活化从而减少细胞损伤。然而,在缺氧条件下,自噬或自噬相关蛋白可能有助于诱导细胞凋亡,而这可能会加重细胞的损伤。此外,凋亡相关蛋白Caspase的活化可以降低自噬相关蛋白的表达,如Atg3、Beclin1蛋白,从而抑制自噬。尽管自噬和细胞凋亡之间的关系已被研究很多年,但潜在的调控机制还没有被清楚地理解。文章对自噬的双重作用和在缺氧条件下自噬和细胞凋亡之间的相互作用和分子调控机制进行综述。Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis caused by hypoxia. Generally autophagy blocks the induction of apoptosis and inhibits the acti- vation of apoptosis associated caspase which could reduce cellular injury. However, autophagy or autophagy relevant proteins may help to induce apoptosis, which could aggravate cell damage under hypoxia condition. In addition, the activation of apop- tosis relevant proteins - caspase can als0 degrade autophagy relevant proteins, such as Atg3, Beclinl protein, inhibiting auto- phagy. Although the relationship between autophagy and apoptosis has been known for rather complex for more than a decade, the underlying regulatory mechanisms have not been deafly understood. This short review discusses and summarizes the dual role of autophagy and the interaction and molecular regulatory mechanisms between autophagy and apoptosis under hypoxia.

关 键 词：自噬 凋亡 缺氧 酶 细胞损伤 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学]