c-Jun N-terminal kinase signaling in cellular senescence
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216305%3A26620%2F23%3APU149207" target="_blank" >RIV/00216305:26620/23:PU149207 - isvavai.cz</a>
Alternative codes found
RIV/62156489:43210/23:43923649 RIV/62690094:18470/23:50020482
Result on the web
<a href="https://link.springer.com/article/10.1007/s00204-023-03540-1" target="_blank" >https://link.springer.com/article/10.1007/s00204-023-03540-1</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1007/s00204-023-03540-1" target="_blank" >10.1007/s00204-023-03540-1</a>
Alternative languages
Result language
angličtina
Original language name
c-Jun N-terminal kinase signaling in cellular senescence
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30107 - Medicinal chemistry
Result continuities
Project
—
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2023
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Archives of Toxicology
ISSN
0340-5761
e-ISSN
1432-0738
Volume of the periodical
97
Issue of the periodical within the volume
8
Country of publishing house
DE - GERMANY
Number of pages
21
Pages from-to
2089-2109
UT code for WoS article
001010658300001
EID of the result in the Scopus database
2-s2.0-85162179424