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.

中文翻译：

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MAPK 对衰老性状的调节。


细胞衰老是响应亚致死损伤而获得的无限期生长停滞的表型，影响正常衰老和与年龄相关的疾病。丝裂原激活蛋白激酶 (MAPK) 能够感知细胞条件的变化，进而引发包括细胞衰老在内的适应性反应。 MAPK 调节许多蛋白质的水平和功能，包括促炎因子以及 p21/p53 和 p16/RB 途径（主要衰老调节轴）中的因子。通过这些作用，MAPK 实现了衰老的关键特征——生长停滞、细胞存活和衰老相关的分泌表型 (SASP)。在这篇综述中，我们总结并讨论了我们目前关于 MAPK 对衰老影响的知识。此外，鉴于消除或抑制衰老细胞可以延长健康寿命，我们讨论了 MAPK 在消除（衰老作用）或抑制（衰老细胞停滞）方面的功能和可能的利用。