• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells
【24h】

Signaling pathways and mechanisms of hypoxia‐induced autophagy in the animal cells

机译：信号传导途径和缺氧诱导的动物细胞自噬的机制

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

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.
机译：缺氧发生在一系列的一系列次级病例中，例如，睡眠障碍，心肌梗死和脑卒中，可以诱导系统的炎症反应。然后，这种反应可以导致广泛的功能障碍和细胞损伤。 Autophagy是一种治疗受损细胞器和蛋白质的营业额的细胞稳态过程可以通过多种形式的细胞内应力引发，例如缺氧，营养剥夺和反应性氧气。该方法的中心是双膜囊泡的形成，从而血管瘤螯合部分的细胞溶溶胶，并将它们递送至溶酶体以进行析出。近年来，已经确定了调节对自噬的细胞反应的几种不同的氧传感途径。例如，缺氧通过激活缺氧诱导因子（HIF）依赖性途径来影响自噬。在慢性和中度缺氧中，自噬通过调解破坏的细胞器和蛋白质来发挥保护作用。此外，三种额外的氧敏感信号通路也与自噬的激活相关。这些包括哺乳动物催盲蛋白（MTOR）激酶的靶标，展开蛋白响应（UPR）和PKCδ-JNK1依赖性途径。与自噬的保护作用相反，在快速和严重的氧气波动期间，自噬可能是有害和诱导细胞死亡。在本综述中，我们强调了最近关于自噬在分子水平和不同缺氧环境下细胞的最终后果的预付款。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号