当前位置: X-MOL 学术Mech. Ageing Dev. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Mitochondria and cellular redox state on the route from ageing to Alzheimer’s disease
Mechanisms of Ageing and Development ( IF 5.3 ) Pub Date : 2020-10-28 , DOI: 10.1016/j.mad.2020.111385
G Abate 1 , M Vezzoli 1 , M Sandri 2 , W Rungratanawanich 1 , M Memo 1 , D Uberti 3
Affiliation  

Several theories have been postulated, trying to explain why and how living organisms age. Despite some controversies and still huge open questions, a growing body of evidence suggest alterations of mitochondrial functionality and redox-homeostasis occur during the ageing process. Oxidative damage and mitochondrial dysfunction do not represent the cause of ageing per se but they have to be analyzed within the complexity of those series of processes occurring during lifespan. The establishment of a crosstalk among them is a shared common feature of many chronic age-related diseases, including neurodegenerative disorders, for which ageing is a major risk factor. The challenge is to understand when and how the interplay between these two systems move towards from normal ageing process to a pathological phenotype. Here in this review, we discuss the crosstalk between mitochondria and cytosolic-ROS. Furthermore, through a visual data mining approach, we attempt to describe the dynamic interplay between mitochondria and cellular redox state on the route from ageing to an AD phenotype.



中文翻译:

从衰老到阿尔茨海默病的过程中的线粒体和细胞氧化还原状态

已经提出了几种理论,试图解释生物体衰老的原因和方式。尽管存在一些争议和巨大的悬而未决的问题,但越来越多的证据表明线粒体功能和氧化还原稳态的改变在衰老过程中发生。氧化损伤和线粒体功能障碍本身并不代表衰老的原因但它们必须在生命周期中发生的一系列过程的复杂性内进行分析。在它们之间建立串扰是许多与年龄相关的慢性疾病的共同特征,包括神经退行性疾病,衰老是其中的主要危险因素。挑战在于了解这两个系统之间的相互作用何时以及如何从正常衰老过程转变为病理表型。在这篇综述中,我们讨论了线粒体和细胞溶质 ROS 之间的串扰。此外,通过可视化数据挖掘方法,我们试图描述从衰老到 AD 表型的过程中线粒体和细胞氧化还原状态之间的动态相互作用。

更新日期:2020-11-02
down
wechat
bug