Charité, Universitätsmedizin Berlin, Institut für Vegetative Physiologie, Berlin, Germany.
J Cell Mol Med. 2009 Sep;13(9A):2770-9. doi: 10.1111/j.1582-4934.2009.00875.x. Epub 2009 Aug 8.
Cells can survive hypoxia/anoxia by metabolic rate depression, which involves lowering of mRNA translation rates in an ATP-dependent manner. By activating anaerobic ATP production (glycolysis), the inhibitory influence on mRNA translation in hypoxia can be abolished. In severe hypoxia, glycolysis cannot fully restore the ATP demand, thus causing a long-lasting inhibition of global protein synthesis. During moderate hypoxia, fermentative ATP production may maintain normal ATP levels. However, an activation of hypoxia tolerance mechanisms, including specific mRNA translation, also takes place. The latter may be attributed to oxygen-dependent (but not ATP dependent) processes such as the activation of the hypoxia-inducible factor cascade. In summary, hypoxia-induced decline in cellular ATP level can be counteracted by suppression of global mRNA translation rate. Sustained protein synthesis seems to be attributed to the activation of specific mRNA translation under long-term hypoxic conditions.
细胞可以通过代谢率降低来在缺氧/缺氧环境中存活，这涉及到以 ATP 依赖的方式降低 mRNA 翻译速率。通过激活无氧 ATP 产生（糖酵解），可以消除缺氧对 mRNA 翻译的抑制作用。在严重缺氧的情况下，糖酵解不能完全恢复 ATP 的需求，从而导致全局蛋白质合成的长期抑制。在中度缺氧的情况下，发酵产生的 ATP 可能会维持正常的 ATP 水平。然而，也会发生缺氧耐受机制的激活，包括特定的 mRNA 翻译。后者可能归因于氧依赖性（而非 ATP 依赖性）的过程，例如缺氧诱导因子级联的激活。总之，细胞内 ATP 水平下降引起的缺氧可以通过抑制全局 mRNA 翻译率来抵消。在长期缺氧条件下，似乎是通过特定 mRNA 翻译的激活来维持持续的蛋白质合成。
