Cordycepin inhibits cell senescence by ameliorating lysosomal dysfunction and inducing autophagy through the AMPK and mTOR–p70S6K pathway,FEBS Open Bio

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Cordycepin inhibits cell senescence by ameliorating lysosomal dysfunction and inducing autophagy through the AMPK and mTOR–p70S6K pathway
FEBS Open Bio ( IF 2.8 ) Pub Date : 2021-08-27 , DOI: 10.1002/2211-5463.13263
Shi Qi Zuo ₁ , Can Li _{2,

3} , Yi Lun Liu _{3,

4} , Yue Hao Tan ₂ , Xing Wan ₁ , Tian Xu ₅ , Qiang Li ₅ , Li Wang ₅ , Yong Li Wu ₅ , Feng Mei Deng ₂ , Bin Tang ₂

Affiliation

Cell senescence is closely related to autophagy. In this article, we identified a natural nucleoside analogue, cordycepin, that has the ability to significantly improve lysosomal function, enhance the activity of the lysosomal representative protease cathepsin B (CTSB), and promote the expression of the functional protein lysosomal-associated membrane protein 2 (LAMP2) on the lysosomal membrane. Cordycepin then restores the damaged autophagy level of aging cells by activating the classic AMPK and mTOR–p70S6K signaling pathways, thus inhibiting cell senescence in an H₂O₂-induced stress-induced premature senescence (SIPS) cell model. This study provides new theoretical support for the further development of cordycepin and clinical antiaging drugs to inhibit cell senescence and suggests that the regulatory mechanisms of lysosomes in senescent cells should be considered when treating age-related diseases.

中文翻译：

虫草素通过改善溶酶体功能障碍和通过 AMPK 和 mTOR-p70S6K 途径诱导自噬来抑制细胞衰老

细胞衰老与自噬密切相关。在本文中，我们鉴定了一种天然核苷类似物虫草素，它能够显着改善溶酶体功能，增强溶酶体代表性蛋白酶组织蛋白酶 B (CTSB) 的活性，并促进功能蛋白溶酶体相关膜蛋白的表达。 2 (LAMP2) 在溶酶体膜上。然后虫草素通过激活经典的 AMPK 和 mTOR-p70S6K 信号通路来恢复衰老细胞受损的自噬水平，从而抑制 H ₂ O _{2中的细胞衰老}-诱导的应激诱导的过早衰老（SIPS）细胞模型。该研究为进一步开发虫草素及临床抗衰老药物抑制细胞衰老提供了新的理论支持，并提示在治疗衰老相关疾病时应考虑衰老细胞中溶酶体的调控机制。

更新日期：2021-10-02

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