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c-Jun N-terminal kinase signaling in aging

Y. Li, L. You, E. Nepovimova, V. Adam, Z. Heger, K. Jomova, M. Valko, Q. Wu, K. Kuca

. 2024 ; 16 (-) : 1453710. [pub] 20240829

Status not-indexed Language English Country Switzerland

Document type Journal Article, Review

Persistent link   https://www.medvik.cz/link/bmc24017944

Aging encompasses a wide array of detrimental effects that compromise physiological functions, elevate the risk of chronic diseases, and impair cognitive abilities. However, the precise underlying mechanisms, particularly the involvement of specific molecular regulatory proteins in the aging process, remain insufficiently understood. Emerging evidence indicates that c-Jun N-terminal kinase (JNK) serves as a potential regulator within the intricate molecular clock governing aging-related processes. JNK demonstrates the ability to diminish telomerase reverse transcriptase activity, elevate β-galactosidase activity, and induce telomere shortening, thereby contributing to immune system aging. Moreover, the circadian rhythm protein is implicated in JNK-mediated aging. Through this comprehensive review, we meticulously elucidate the intricate regulatory mechanisms orchestrated by JNK signaling in aging processes, offering unprecedented molecular insights with significant implications and highlighting potential therapeutic targets. We also explore the translational impact of targeting JNK signaling for interventions aimed at extending healthspan and promoting longevity.

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$a Aging encompasses a wide array of detrimental effects that compromise physiological functions, elevate the risk of chronic diseases, and impair cognitive abilities. However, the precise underlying mechanisms, particularly the involvement of specific molecular regulatory proteins in the aging process, remain insufficiently understood. Emerging evidence indicates that c-Jun N-terminal kinase (JNK) serves as a potential regulator within the intricate molecular clock governing aging-related processes. JNK demonstrates the ability to diminish telomerase reverse transcriptase activity, elevate β-galactosidase activity, and induce telomere shortening, thereby contributing to immune system aging. Moreover, the circadian rhythm protein is implicated in JNK-mediated aging. Through this comprehensive review, we meticulously elucidate the intricate regulatory mechanisms orchestrated by JNK signaling in aging processes, offering unprecedented molecular insights with significant implications and highlighting potential therapeutic targets. We also explore the translational impact of targeting JNK signaling for interventions aimed at extending healthspan and promoting longevity.
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$a You, Li $u College of Physical Education and Health, Chongqing College of International Business and Economics, Chongqing, China
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$a Nepovimova, Eugenie $u Department of Chemistry, Faculty of Science, University of Hradec Králové, Hradec Králové, Czechia
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$a Adam, Vojtech $u Department of Chemistry and Biochemistry, Mendel University in Brno, Brno, Czechia
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$a Heger, Zbynek $u Department of Chemistry and Biochemistry, Mendel University in Brno, Brno, Czechia
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$a Jomova, Klaudia $u Department of Chemistry, Faculty of Natural Sciences and Informatics, Constantine the Philosopher University in Nitra, Nitra, Slovakia
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$a Valko, Marian $u Faculty of Chemical and Food Technology, Slovak University of Technology, Bratislava, Slovakia
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$a Wu, Qinghua $u College of Life Science, Yangtze University, Jingzhou, China $u Department of Chemistry, Faculty of Science, University of Hradec Králové, Hradec Králové, Czechia
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$a Kuca, Kamil $u Department of Chemistry, Faculty of Science, University of Hradec Králové, Hradec Králové, Czechia $u Faculty of Chemical and Food Technology, Slovak University of Technology, Bratislava, Slovakia
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