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霍奇卡的“缺氧防御策略”与氧代谢途径的发展

Hochachka's "Hypoxia Defense Strategies" and the development of the pathway for oxygen.

作者信息

Land Stephen C

机构信息

Division of Maternal and Child Health Sciences, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, Scotland, UK.

出版信息

Comp Biochem Physiol B Biochem Mol Biol. 2004 Nov;139(3):415-33. doi: 10.1016/j.cbpc.2004.02.016.

Abstract

Hochachka's "Hypoxia Defense Strategies" identify oxygen signalling, metabolic arrest, channel arrest and coordinated suppression of ATP turnover rates as key factors that determine the ability of organisms to survive exposure to chronic hypoxia. In this review, I assess the developmental role played by these phenomena in the morphogenesis of the gas exchange tissues that define the pathway for oxygen transport to cytochrome c oxidase. Key areas of regulation lie in: (I) the suppression of fetal mitochondrial oxidative function in hand with mitochondrial biogenesis (metabolic arrest), (II) the role of hypoxia-driven oxygen signalling pathways in directing the scope of non-differentiated stem cell proliferation in placenta and lung development and (III) the regulation of epithelial fluid secretion/absorption in the lung through the oxygen-dependent modulation of Na+ conductance pathways. The identification of developmental roles for Hochachka's "Hypoxia Defense Strategies" in directing the morphogenesis of gas exchange structures bears with it the implication that these strategies are fundamental to establishing the scope for aerobic metabolic performance throughout life.

摘要

霍奇卡的“缺氧防御策略”确定了氧信号传导、代谢停滞、通道停滞以及ATP周转率的协同抑制是决定生物体在长期缺氧环境中生存能力的关键因素。在这篇综述中,我评估了这些现象在气体交换组织形态发生过程中所起的发育作用,这些组织定义了氧气输送到细胞色素c氧化酶的途径。关键的调控领域包括:(I)与线粒体生物发生(代谢停滞)同步抑制胎儿线粒体氧化功能;(II)缺氧驱动的氧信号通路在指导胎盘和肺发育中未分化干细胞增殖范围方面的作用;(III)通过对钠电导途径的氧依赖性调节来调控肺上皮液体的分泌/吸收。确定霍奇卡的“缺氧防御策略”在指导气体交换结构形态发生中的发育作用意味着这些策略对于确立整个生命过程中有氧代谢表现的范围至关重要。

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