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A mitochondrially targeted compound delays aging in yeast through a mechanism linking mitochondrial membrane lipid metabolism to mitochondrial redox biology

机译:线粒体靶向化合物通过将线粒体膜脂质代谢与线粒体氧化还原生物学联系起来的机制延迟酵母的衰老

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摘要

A recent study revealed a mechanism of delaying aging in yeast by a natural compound which specifically impacts mitochondrial redox processes. In this mechanism, exogenously added lithocholic bile acid enters yeast cells, accumulates mainly in the inner mitochondrial membrane, and elicits an age-related remodeling of phospholipid synthesis and movement within both mitochondrial membranes. Such remodeling of mitochondrial phospholipid dynamics progresses with the chronological age of a yeast cell and ultimately causes significant changes in mitochondrial membrane lipidome. These changes in the composition of membrane phospholipids alter mitochondrial abundance and morphology, thereby triggering changes in the age-related chronology of such longevity-defining redox processes as mitochondrial respiration, the maintenance of mitochondrial membrane potential, the preservation of cellular homeostasis of mitochondrially produced reactive oxygen species, and the coupling of electron transport to ATP synthesis.
机译:最近的一项研究揭示了一种通过天然化合​​物延缓酵母衰老的机制,该化合物会特别影响线粒体的氧化还原过程。在这种机制下,外源添加的石脑胆汁酸进入酵母细胞,主要在线粒体内膜中积累,并引起与年龄相关的磷脂合成和线粒体膜内运动的重塑。线粒体磷脂动力学的这种重塑随着酵母细胞的时间年龄而发展,并最终导致线粒体膜脂质组的显着变化。膜磷脂成分的这些变化改变了线粒体的丰度和形态,从而触发了与年龄相关的时序变化,如长寿的氧化还原过程,如线粒体呼吸作用,线粒体膜电位的维持,线粒体产生的反应性的细胞稳态的保持氧物种,以及电子传输与ATP合成的耦合。

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