The regulatory role of PI3K in ageing-related diseases

Ageing is a physiological/pathological process accompanied by the progressive damage of cell function, triggering various ageing-related disorders. Phosphatidylinositol 3-kinase (PI3K), which serves as one of the central regulators of ageing, is closely associated with cellular characteristics or mo...

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Veröffentlicht in:Ageing research reviews 2023-07, Vol.88, p.101963-101963, Article 101963
Hauptverfasser: Liu, Yanqing, Liu, Qiong, Zhang, Zhe, Yang, Yaru, Zhou, Yazhe, Yan, Huanle, Wang, Xin, Li, Xiaoru, Zhao, Jing, Hu, Jingyan, Yang, Shulin, Tian, Yifan, Yao, Yu, Qiu, Zhenye, Song, Yanbin, Yang, Yang
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Sprache:eng
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Zusammenfassung:Ageing is a physiological/pathological process accompanied by the progressive damage of cell function, triggering various ageing-related disorders. Phosphatidylinositol 3-kinase (PI3K), which serves as one of the central regulators of ageing, is closely associated with cellular characteristics or molecular features, such as genome instability, telomere erosion, epigenetic alterations, and mitochondrial dysfunction. In this review, the PI3K signalling pathway was firstly thoroughly explained. The link between ageing pathogenesis and the PI3K signalling pathway was then summarized. Finally, the key regulatory roles of PI3K in ageing-related illnesses were investigated and stressed. In summary, we revealed that drug development and clinical application targeting PI3K is one of the focal points for delaying ageing and treating ageing-related diseases in the future. •Ageing is a complex process that copes with several cellular processes, including genomic instability, oxidative stress, etc.•PI3K has three subtypes and mediates multiple downstream molecules such as mTOR and FOXO.•PI3K is involved in ageing-related biological processes and plays a regulatory role in ageing-related diseases.•The study of PI3K subtypes is the key to developing the drugs that target PI3K to combat ageing-related diseases.
ISSN:1568-1637
1872-9649
DOI:10.1016/j.arr.2023.101963