Douglas Robert M, Haddad Gabriel G
Department of Pediatrics, University of California San Diego, and Rady Children's Hospital-San Diego, San Diego, La Jolla, CA, USA.
Physiology (Bethesda). 2008 Dec;23:333-49. doi: 10.1152/physiol.00023.2008.
Chronic intermittent or episodic hypoxia, as occurs during a number of disease states, can have devastating effects, and prolonged exposure to this hypoxia can result in cell injury or cell death. Indeed, intermittent hypoxia activates a number of signaling pathways that are involved in oxygen sensing, oxidative stress, metabolism, catecholamine biosynthesis, and immune responsiveness. The cumulative effect of these processes over time can undermine cell integrity and lead to a decline in function. Furthermore, the ability to respond adequately to various stressors is hampered, and this is traditionally defined as premature aging or senescence. This review highlights recent advances in our understanding of the cellular and molecular mechanisms that are involved in the response to intermittent hypoxia and the potential interplay among various pathways that may accelerate the aging process.
慢性间歇性或发作性缺氧，如在多种疾病状态下所发生的那样，会产生毁灭性影响，长时间暴露于这种缺氧状态会导致细胞损伤或细胞死亡。事实上，间歇性缺氧会激活一系列参与氧感知、氧化应激、代谢、儿茶酚胺生物合成和免疫反应的信号通路。随着时间的推移，这些过程的累积效应会破坏细胞完整性并导致功能下降。此外，对各种应激源做出充分反应的能力也会受到阻碍，这传统上被定义为早衰或衰老。本综述重点介绍了我们对间歇性缺氧反应中涉及的细胞和分子机制以及可能加速衰老过程的各种途径之间潜在相互作用的最新认识进展。
