Regulation of Cellular Gas Exchange, Oxygen Sensing, and Metabolic Control
Regulation of Cellular Gas Exchange, Oxygen Sensing, and Metabolic Control
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DOI：
10.1002/cphy.c120030
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发表时间：
2013-07-01
影响因子：
5.8
通讯作者：
Gladden, L. B.
中科院分区：
文献类型：
--
作者：
Clanton, T. L.;Hogan, M. C.;Gladden, L. B.
细胞必须持续监测其对ATP利用的代谢需求，并将其与线粒体呼吸吸收O-2的能力结合起来。当O-2的摄取和输送走出动态平衡时，细胞有复杂多样的感知和反应系统进行补偿。在这篇综述中，我们探讨了细胞内O-2和气体扩散的生物物理机制，细胞内O-2是如何调节的，细胞内O-2水平是如何被感知的，以及感知系统是如何影响线粒体呼吸和代谢途径的变化的。特别注意O-2如何影响电池的氧化还原状态，以及NO、H_2S和CO浓度。我们还探讨了这些药物如何影响气体交换的各个方面，并激活促进生存的急性信号通路。还详细讨论了气体交换的两种挑战：当氧气不足可用于呼吸时(缺氧)和当代谢需求测试气体交换的极限时(锻炼骨骼肌)。这篇综述也集中在Hochachka和他的同事所表达的最初的“耐缺氧统一理论”的背景下对急性缺氧的反应。它包括对线粒体电子传递的调节、代谢抑制、代谢途径的转变以及阻止膜电位崩溃和核凋亡的细胞生存途径的重新招募。关于运动，讨论的问题涉及代谢率的氧-2敏感性，运动中的氧-2动力学，以及有效氧对糖酵解和乳酸产生的影响。(C)2013美国生理学会。
Cells must continuously monitor and couple their metabolic requirements for ATP utilization with their ability to take up O-2 for mitochondrial respiration. When O-2 uptake and delivery move out of homeostasis, cells have elaborate and diverse sensing and response systems to compensate. In this review, we explore the biophysics of O-2 and gas diffusion in the cell, how intracellular O-2 is regulated, how intracellular O-2 levels are sensed and how sensing systems impact mitochondrial respiration and shifts in metabolic pathways. Particular attention is paid to how O-2 affects the redox state of the cell, as well as the NO, H2S, and CO concentrations. We also explore how these agents can affect various aspects of gas exchange and activate acute signaling pathways that promote survival. Two kinds of challenges to gas exchange are also discussed in detail: when insufficient O-2 is available for respiration (hypoxia) and when metabolic requirements test the limits of gas exchange (exercising skeletal muscle). This review also focuses on responses to acute hypoxia in the context of the original "unifying theory of hypoxia tolerance" as expressed by Hochachka and colleagues. It includes discourse on the regulation of mitochondrial electron transport, metabolic suppression, shifts in metabolic pathways, and recruitment of cell survival pathways preventing collapse of membrane potential and nuclear apoptosis. Regarding exercise, the issues discussed relate to the O-2 sensitivity of metabolic rate, O-2 kinetics in exercise, and influences of available O-2 on glycolysis and lactate production. (C) 2013 American Physiological Society.