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The mitochondrial Na+/Ca2+ exchanger NCLX is implied in the activation of hypoxia-inducible factors
Redox Biology ( IF 10.7 ) Pub Date : 2024-09-19 , DOI: 10.1016/j.redox.2024.103364
Carmen Choya-Foces, Elisa Navarro, Cristóbal de los Ríos, Manuela G. López, Javier Egea, Pablo Hernansanz-Agustín, Antonio Martínez-Ruiz

Eukaryotic cells and organisms depend on oxygen for basic living functions, and they display a panoply of adaptations to situations in which oxygen availability is diminished (hypoxia). A number of these responses in animals are mediated by changes in gene expression programs directed by hypoxia-inducible factors (HIFs), whose main mechanism of stabilization and functional activation in response to decreased cytosolic oxygen concentration was elucidated two decades ago. Human acute responses to hypoxia have been known for decades, although their precise molecular mechanism for oxygen sensing is not fully understood. It is already known that a redox component, linked with reactive oxygen species (ROS) production of mitochondrial origin, is implied in these responses. We have recently described a mechanism by which the mitochondrial sodium/calcium exchanger, NCLX, participates in mitochondrial electron transport chain regulation and ROS production in response to acute hypoxia.

中文翻译:


线粒体 Na + / Ca2 + 交换剂 NCLX 暗示了缺氧诱导因子的激活



真核细胞和生物体依赖氧气来实现基本生活功能,它们对氧气可用性减少(缺氧)的情况表现出一系列适应性。动物中的许多这些反应是由缺氧诱导因子 (HIF) 指导的基因表达程序的变化介导的,其响应胞质氧浓度降低的稳定和功能激活的主要机制在二十年前就已阐明。人类对缺氧的急性反应已经为人所知几十年,尽管它们对氧感应的确切分子机制尚不完全清楚。众所周知,这些反应中隐含了与线粒体来源的活性氧 (ROS) 产生有关的氧化还原成分。我们最近描述了一种机制,线粒体钠/钙交换剂 NCLX 参与线粒体电子传递链调节和 ROS 产生以响应急性缺氧。
更新日期:2024-09-19
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