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Protein oxidation in aging: endoplasmic reticulum as a target

机译：老化中的蛋白质氧化：以内质网为目标

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Oxidatively modified proteins have been shown to correlate with the age of an organism or its tissues. An increase in tissue-susceptibility to experimentally induced protein oxidation not only depends on tissue type and age, but also on the maximum lifespan potential of the species. A general, although tissue dependent, decline in anti-oxidative defenses during aging may very well be responsible for this difference in vulnerability. In addition, the level of protein modifications also depends on the nature and the subcellular localization of the proteins involved. Damage to the endoplasmic reticulum (ER), and its subsequent impaired functionality may be involved in the process of aging. This is suggested by; (1) an upregulation of ER stress-response chaperones, (2) a preferential oxidation of ER-resident proteins and, (3) a disturbance of calcium homeostasis. Therefore, this review will focus on the putative involvement of the oxidized endoplasmic reticulum in the process of aging.
机译：已经证明氧化修饰的蛋白质与生物体或其组织的年龄相关。组织对实验诱导的蛋白质氧化的敏感性增加不仅取决于组织类型和年龄，还取决于物种的最大寿命潜力。一般的（尽管是组织依赖性的）衰老过程中抗氧化防御能力的下降很可能是造成这种脆弱性差异的原因。另外，蛋白质修饰的水平还取决于所涉及蛋白质的性质和亚细胞定位。内质网（ER）的损坏及其随后的功能受损可能与衰老过程有关。这是由建议的; （1）内质网应激反应伴侣的上调，（2）内质网驻留蛋白的优先氧化，（3）钙稳态的干扰。因此，本综述将集中于氧化内质网在衰老过程中的可能参与。

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