Cordycepin inhibits cell senescence by ameliorating lysosomal dysfunction and inducing autophagy through the AMPK and mTOR–p70S6K pathway
Autor: | Xing Wan, Yue Hao Tan, Qiang Li, Li Wang, Yong Li Wu, Yi-Lun Liu, Shi Qi Zuo, Feng Mei Deng, Bin Tang, Tian Xu, Can Li |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Senescence
autophagy QH301-705.5 AMPK signaling pathways AMP-Activated Protein Kinases General Biochemistry Genetics and Molecular Biology Cathepsin B chemistry.chemical_compound Biology (General) Cellular Senescence Research Articles PI3K/AKT/mTOR pathway cordycepin lysosomal function LAMP2 Deoxyadenosines Cordycepin Chemistry TOR Serine-Threonine Kinases Autophagy Ribosomal Protein S6 Kinases 70-kDa AMPK lysosomal protease Cell biology cell senescence Lysosomes Cell aging Research Article |
Zdroj: | FEBS Open Bio, Vol 11, Iss 10, Pp 2705-2714 (2021) FEBS Open Bio |
ISSN: | 2211-5463 |
Popis: | 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. Here, we show that cordycepin enhances the expression of cathepsin B (CTSB) and lysosomal‐associated membrane protein 2 (LAMP2) and mediates the AMPK and mTOR‐p70S6K pathways to restore autophagy in aging cells. |
Databáze: | OpenAIRE |
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