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Review
. 2020 Apr;42(2):397-408.
doi: 10.1007/s11357-020-00183-3. Epub 2020 Apr 16.

Regulation of senescence traits by MAPKs

Carlos Anerillas  1 , Kotb Abdelmohsen  1 , Myriam Gorospe  2
Affiliations
Review

Regulation of senescence traits by MAPKs

Carlos Anerillas et al. Geroscience. 2020 Apr.

Abstract

A phenotype of indefinite growth arrest acquired in response to sublethal damage, cellular senescence affects normal aging and age-related disease. Mitogen-activated protein kinases (MAPKs) are capable of sensing changes in cellular conditions, and in turn elicit adaptive responses including cell senescence. MAPKs modulate the levels and function of many proteins, including proinflammatory factors and factors in the p21/p53 and p16/RB pathways, the main senescence-regulatory axes. Through these actions, MAPKs implement key traits of senescence-growth arrest, cell survival, and the senescence-associated secretory phenotype (SASP). In this review, we summarize and discuss our current knowledge of the impact of MAPKs in senescence. In addition, given that eliminating or suppressing senescent cells can improve health span, we discuss the function and possible exploitation of MAPKs in the elimination (senolysis) or suppression (senostasis) of senescent cells.

Keywords: ERK; Gene expression programs; JNK; SASP; Senescence; p38.

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Figures

Fig. 1
Fig. 1
Known implications of MAPK pathways in cellular senescence traits. After exposure to senescence-inducing stimuli, MAPK pathways (mainly p38 and ERK1/2) drive the implementation of the senescence phenotype. MAPKs exert direct control over the main senescence traits—cell survival, cell cycle arrest, and the senescence-associated secretory phenotype (SASP). The main MAPK regulatory events thus far implicated in senescence are indicated.
See this image and copyright information in PMC

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