Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA.
Dev Cell. 2018 Jan 22;44(2):139-163. doi: 10.1016/j.devcel.2017.12.020.
There exists a phenomenon in aging research whereby early life stress can have positive impacts on longevity. The mechanisms underlying these observations suggest a robust, long-lasting induction of cellular defense mechanisms. These include the various unfolded protein responses of the endoplasmic reticulum (ER), cytosol, and mitochondria. Indeed, ectopic induction of these pathways, in the absence of stress, is sufficient to increase lifespan in organisms as diverse as yeast, worms, and flies. Here, we provide an overview of the protein quality control mechanisms that operate in the cytosol, mitochondria, and ER and discuss how they affect cellular health and viability during stress and aging.
衰老研究中存在一种现象，即早期生活压力可能对长寿产生积极影响。这些观察结果背后的机制表明，细胞防御机制得到了强大而持久的诱导。其中包括内质网（ER）、细胞质和线粒体的各种未折叠蛋白反应。事实上，在没有压力的情况下异位诱导这些途径足以增加酵母、蠕虫和苍蝇等不同生物的寿命。在这里，我们提供了一个概述细胞质、线粒体和 ER 中运行的蛋白质质量控制机制，并讨论了它们在压力和衰老过程中如何影响细胞健康和活力。
