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c-Jun N-terminal kinase signaling in cellular senescence

文献类型： 外文期刊

作者： Deng, Ying 1 ; Adam, Vojtech 4 ; Nepovimova, Eugenie 3 ; Heger, Zbynek 4 ; Valko, Marian 6 ; Wu, Qinghua 1 ; Wei, Wei 2 ; Kuca, Kamil 3 ;

作者机构： 1.Yangtze Univ, Coll Life Sci, Jingzhou 434025, Peoples R China

2.Zhejiang Acad Agr Sci, State Key Lab Managing Biot & Chem Threats Qual &, Key Lab Traceabil Agr Genet Modified Organisms, Minist Agr & Rural Affairs, Hangzhou 310021, Peoples R China

3.Univ Hradec Kralove, Fac Sci, Dept Chem, Hradec Kralove 50003, Czech Republic

4.Mendel Univ Brno, Dept Chem & Biochem, Brno 61300, Czech Republic

5.Brno Univ Technol, Cent European Inst Technol, Brno 60200, Czech Republic

6.Slovak Univ Technol Bratislava, Fac Chem & Food Technol, Bratislava 81237, Slovakia

7.Univ Granada, Andalusian Res Inst Data Sci & Computat Intelligen, Granada, Spain

关键词： JNK; Cell senescence; Hypoxia; PARP1; Anti-aging

期刊名称：ARCHIVES OF TOXICOLOGY （ 影响因子：6.1； 五年影响因子：5.7 ）

ISSN： 0340-5761

年卷期： 2023 年 97 卷 8 期

页码：

收录情况： SCI

摘要： Cellular senescence leads to decreased tissue regeneration and inflammation and is associated with diabetes, neurodegenerative diseases, and tumorigenesis. However, the mechanisms of cellular senescence are not fully understood. Emerging evidence has indicated that c-Jun N-terminal kinase (JNK) signaling is involved in the regulation of cellular senescence. JNK can downregulate hypoxia inducible factor-1 alpha to accelerate hypoxia-induced neuronal cell senescence. The activation of JNK inhibits mTOR activity and triggers autophagy, which promotes cellular senescence. JNK can upregulate the expression of p53 and Bcl-2 and accelerates cancer cell senescence; however, this signaling also mediates the expression of amphiregulin and PD-LI to achieve cancer cell immune evasion and prevents their senescence. The activation of JNK further triggers forkhead box O expression and its target gene Jafrac1 to extend the lifespan of Drosophila. JNK can also upregulate the expression of DNA repair protein poly ADP-ribose polymerase 1 and heat shock protein to delay cellular senescence. This review discusses recent advances in understanding the function of JNK signaling in cellular senescence and includes a comprehensive analysis of the molecular mechanisms underlying JNK-mediated senescence evasion and oncogene-induced cellular senescence. We also summarize the research progress in anti-aging agents that target JNK signaling. This study will contribute to a better understanding of the molecular targets of cellular senescence and provides insights into anti-aging, which may be used to develop drugs for the treatment of aging-related diseases.

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