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细胞自噬是细胞依赖溶酶体的分解代谢过程,能降解受损蛋白、衰老或损伤的细胞器等细胞结构,可被多种应激所触发。在营养匮乏或组织缺血缺氧等应激条件下,自噬作为相应的代谢过程通过提供代用能源及清除功能异常的细胞器及蛋白质类维持细胞存活。缺血缺氧是细胞自噬激活的重要诱因之一,自噬的适度增强可促进细胞在缺血缺氧等状态下的存活。该文就细胞自噬的分子机制、缺血缺氧状态下自噬调控通路的调节机制及其分子水平检测技术的研究进展予以综述。
Cell autophagy is a cell-dependent lysosomal catabolism process that can degrade damaged proteins, cellular structures such as aging or damaged organelles, and can be triggered by a variety of stresses. In the condition of lack of nutrition or tissue hypoxia and other stress, autophagy as the corresponding metabolic process to maintain cell survival by providing alternative energy and removing abnormally functioning organelles and proteins. Ischemia and hypoxia are one of the important inducing factors of autophagic activation. The moderate enhancement of autophagy can promote the survival of cells in the state of hypoxia and hypoxia. This review summarizes the molecular mechanisms of autophagy, the regulatory mechanisms of autophagy regulatory pathways under hypoxia and hypoxia, and the molecular level of these mechanisms.