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- Title
Signaling pathways and mechanisms of hypoxia-induced autophagy in the animal cells.
- Authors
Fang, Yungyun; Tan, Jin; Zhang, Qiang
- Abstract
Hypoxia occurs in a series of supraphysiological circumstances, for instance, sleep disorders, myocardial infarction and cerebral stroke, that can induce a systematic inflammatory response. Such a response may then lead to a widespread dysfunction and cell injury. Autophagy, a cellular homeostatic process that governs the turnover of damaged organelles and proteins, can be triggered by multiple forms of extra- and intracellular stress, for example, hypoxia, nutrient deprivation and reactive oxygen specie. Central to this process is the formation of double-membrane vesicles, thereby autophagosomes sequester portions of cytosol and deliver them to the lysosomes for a breakdown. In recent years, several distinct oxygen-sensing pathways that regulate the cellular response to autophagy have been defined. For instance, hypoxia influences autophagy in part through the activation of the hypoxia-inducible factor (HIF)-dependent pathways. In chronic and moderate hypoxia, autophagy plays a protective role by mediating the removal of the damaged organelles and protein. Moreover, three additional oxygen-sensitive signaling pathways are also associated with the activation of autophagy. These include mammalian target of rapamycin (mTOR) kinase, unfolded protein response (UPR)- and PKCδ-JNK1-dependent pathways. Contrary to the protective effects of autophagy, during rapid and severe oxygen fluctuations, autophagy may be detrimental and induce cell death. In this review, we highlight a serious of recent advances on how autophagy is regulated at the molecular level and on final consequences of cell under different hypoxic environment.
- Subjects
CELL physiology; AUTOPHAGY; CELLULAR signal transduction; PATHOPHYSIOLOGY of anoxemia; SLEEP disorders; MYOCARDIAL infarction
- Publication
Cell Biology International, 2015, Vol 39, Issue 8, p891
- ISSN
1065-6995
- Publication type
Article
- DOI
10.1002/cbin.10463