MAPKs 调控衰老相关表型。
Regulation of senescence traits by MAPKs.
机构信息
Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD, 21224, USA.
出版信息
Geroscience. 2020 Apr;42(2):397-408. doi: 10.1007/s11357-020-00183-3. Epub 2020 Apr 16.
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.
摘要
一种对亚致死性损伤产生的无限期生长停滞的表型，细胞衰老会影响正常衰老和与年龄相关的疾病。丝裂原活化蛋白激酶（MAPK）能够感知细胞状态的变化，并反过来引发适应性反应，包括细胞衰老。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 通路中的因子，这是主要的衰老调节轴。通过这些作用，MAPK 实现了衰老-生长停滞、细胞存活和衰老相关分泌表型（SASP）的关键特征。在这篇综述中，我们总结和讨论了我们目前对 MAPK 在衰老中的作用的认识。此外，鉴于消除或抑制衰老细胞可以改善健康跨度，我们讨论了 MAPK 在衰老细胞的消除（衰老细胞溶解）或抑制（衰老细胞静止）中的功能和可能的利用。
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