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Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Stress-activated MAP kinase cascades in cellular senescence
Junichi Maruyama1, Isao Naguro, Kohsuke Takeda
1Laboratory of Cell Signaling, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Current Medicinal Chemistry
|April 10, 2009
Summary
Cellular senescence, a state of irreversible cell cycle arrest, prevents cancer but can drive age-related diseases when cells accumulate. This review highlights stress-induced signaling pathways, particularly JNK and p38 MAPK, regulating senescence.
Area of Science:
- Cellular and Molecular Biology
- Aging Research
- Oncology
Background:
- Normal somatic cells undergo cell cycle arrest (cellular senescence) due to telomere shortening or DNA damage.
- Cellular senescence acts as a tumor suppressor mechanism by preventing damaged cells from proliferating.
- However, the accumulation of senescent cells contributes to tissue dysfunction and age-related diseases.
Purpose of the Study:
- To review the signaling pathways regulating stress-induced cellular senescence.
- To emphasize the roles of c-Jun N-terminal kinases (JNK) and p38 MAPK cascades in this process.
Main Methods:
- This review synthesizes existing research on cellular senescence.
- Focuses on molecular signaling pathways, including stress-activated mitogen-activated protein kinases (MAPK).
Main Results:
- Cellular senescence is triggered by telomere shortening, DNA damage, and mitogenic signals.
- While senescence suppresses tumors, its accumulation leads to age-related pathologies.
- Stress-activated MAPK pathways, specifically JNK and p38, are crucial regulators of stress-induced senescence.
Conclusions:
- Understanding stress-induced senescence signaling is vital for addressing age-related diseases.
- Targeting JNK and p38 MAPK pathways may offer therapeutic strategies for senescence-related conditions.
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