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Is (your cellular response to) stress killing you?

机译:(您对细胞的反应)压力会杀死您吗?

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摘要

Free radicals provide a generally accepted explanation for age-related decline in tissue function. However, the free radical hypothesis does not provide a mechanistic course of action to explain exactly how damage to macromolecules translates into the recognizable pathophysiology of aged organisms. Recent advances in the fields of DNA damage and cellular senescence point towards a substantial role for the DNA damage response, rather than DNA mutations per se, in the genesis of cellular and/or tissue damage. Furthermore, several studies suggest that protein damage can be at least as important as DNA damage in bringing about the aging phenotype. Here we propose that a "protein damage response," namely the ER/UPR (endoplasmic reticulum/unfolded protein) stress response is likely to play an important role in the aging process.
机译:自由基为年龄相关的组织功能下降提供了公认的解释。但是,自由基假说并未提供机制的作用机理来确切解释大分子的损害如何转化为衰老生物体的可识别病理生理。 DNA损伤和细胞衰老领域的最新进展表明,在细胞和/或组织损伤的发生中,DNA损伤反应起着重要作用,而不是DNA突变本身。此外,一些研究表明,蛋白质损伤在引起衰老表型方面至少与DNA损伤一样重要。在这里,我们提出“蛋白质损伤反应”,即ER / UPR(内质网/未折叠蛋白)应激反应可能在衰老过程中起重要作用。

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