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首页> 外文期刊>Current pharmaceutical design >Inflamm-aging, cytokines and aging: state of the art, new hypotheses on the role of mitochondria and new perspectives from systems biology.
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Inflamm-aging, cytokines and aging: state of the art, new hypotheses on the role of mitochondria and new perspectives from systems biology.

机译:炎症老化,细胞因子和衰老:最新技术,关于线粒体作用的新假设以及系统生物学的新观点。

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摘要

In this article we summarise present knowledge on the role of pro-inflammatory cytokines on chronic inflammation leading to organismal aging, a phenomenon we proposed to call "inflamm-aging". In particular, we review genetic data regarding polymorphisms of genes encoding for cytokines and proteins involved in natural immunity (such as Toll-like Receptors and Heat Shock Proteins) obtained from large population studies including young, old and very old people in good health status or affected by age-related diseases such as Alzheimer's Disease and Type II Diabetes. On the whole, despite some controversial results, the available data are in favour of the hypothesis that pro-inflammatory cytokines play an important role in aging and longevity. Further, we present a possible hypothesis to reconcile energetic dysfunction, including mitochondria, and inflamm-aging. New perspectives for future studies, including phylogenetic studies in animal models and in silico studies on mathematical and bioinformatic models inspired by the systems biology approach, are also proposed.
机译:在本文中,我们总结了有关促炎细胞因子在导致机体衰老的慢性炎症中的作用的现有知识,我们将这种现象称为“炎症衰老”。特别是,我们审查了有关遗传数据的遗传数据,这些基因编码自然免疫中涉及的细胞因子和蛋白质(例如Toll样受体和热休克蛋白)的基因多态性,这些基因是通过大量人群研究(包括健康状况良好的年轻人,老年人和非常老年人)获得的。受年龄相关疾病(例如阿尔茨海默氏病和II型糖尿病)的影响。总体而言,尽管得出了一些有争议的结果,但现有数据支持了促炎性细胞因子在衰老和长寿中起重要作用的假说。此外,我们提出了一个可能的假设来调和包括线粒体和炎症衰老在内的能量功能障碍。还提出了用于未来研究的新观点,包括动物模型的系统发育研究以及受系统生物学方法启发进行的数学和生物信息模型的计算机模拟研究。

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