摘要
低氧是一种典型的应激环境,细胞在低氧条件下能量和氧化代谢发生改变,其中线粒体产生的大量活性氧严重威胁细胞的存活.线粒体自噬是近年来被发现的细胞适应低氧的一种适应性代谢反应.细胞在低氧条件下能通过上调低氧诱导因子1(HIF-1),激活BNIP3/BNIP3L及Beclin-1介导的通路诱导线粒体自噬,最终减少ROS的产生,促进细胞的存活,使机体产生低氧适应.综述了线粒体自噬在低氧适应中的作用及其机制.
Hypoxia is a representative stress environment,under which cell energy and oxidative metabolism change a lot.Among the product of metabolism,reactive oxygen species(ROS) which generate from mitochondria under hypoxia seriously threaten cell survive.Mitophagy was recently found as an adaptive metabolic response to hypoxia.Cell induces mitophagy by the pathway mediated by BNIP3/BNIP3L and Beclin-1 that are activated by up-regulation of HIF-1 under hypoxia,then reduces the production of ROS,and ultimately promotes cell survival.This process leads to the adaptation of organism to hypoxia.In this paper,we will overview the role and the mechanism of mitophagy in adaptation to hypoxia.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2012年第3期217-223,共7页
Progress In Biochemistry and Biophysics
基金
国家重点基础研究发展计划(973)(2011CB910800
2012CB518200)
国家自然科学基金(81000856
81071066)资助项目~~