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c-Jun N-终端酶在细胞衰老中的信号传递

Ying Deng¹, Vojtech Adam^2,3, Eugenie Nepovimova⁴

¹College of Life Science, Yangtze University, Jingzhou, 434025, China.

Archives of toxicology

|June 19, 2023

概括

c-Jun N-终端激酶 (JNK) 途径在细胞衰老中起着双重作用,影响衰老和与年龄相关的疾病. 了解JNK信号为抗衰老疗法和与衰老有关的疾病的治疗提供了新的途径.

科学领域:

细胞和分子生物学细胞和分子生物学
衰老研究研究衰老研究
信号转导信号转导

背景情况:

细胞衰老有助于衰老和糖尿病和癌症等疾病.
调节细胞衰老的精确机制仍然不完全理解.
新出现的证据表明c-Jun N-终端激酶 (JNK) 在衰老途径中的信号传递.

研究的目的:

审查了解JNK信号传递在细胞衰老中的作用的最新进展.
分析JNK介导衰老逃避和基因诱导衰老的分子机制.
总结针对JNK信号的抗衰老剂的研究.

主要方法:

对JNK信号传递和细胞衰老研究的文献综述.
通过JNK调节的分子通路的分析,包括HIF-1α,mTOR,p53,Bcl-2,安菲瑞古林,PD-L1,FOXO,Jafrac1,PARP1和HSPs.
与衰老逃避和瘤基因诱导衰老相关的发现的综合.

主要成果:

简基因信号传递具有复杂的作用,在某些情况下促进衰老 (例如,缺氧,癌症),在其他情况下抑制衰老 (例如,Drosophila的寿命延长,DNA修复).
通过不同的点,JNK影响衰老,影响细胞循环,炎症,免疫逃避和DNA修复.
矛盾的是,JNK激活可以通过免疫逃避机制在癌细胞中促进衰老逃避.

结论:

简基因信号传递是细胞衰老的关键调节者,具有上下文依赖的影响.
准JNK通路有可能开发新的抗衰老策略和治疗与衰老相关的疾病.
对JNK分子点的进一步研究对于推进抗衰老疗法至关重要.

关键词:

抗衰老的抗衰老的抗衰老的细胞衰老细胞衰老氧气过低是因为缺氧.在JNK中,JNK就是JNK.PARP1 的第一部分.

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