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观点:靶向JAK/STAT信号通路对抗与年龄相关的功能障碍。

Perspective: Targeting the JAK/STAT pathway to fight age-related dysfunction.

作者信息

Xu Ming, Tchkonia Tamar, Kirkland James L

机构信息

Robert and Arlene Kogod Center on Aging, Mayo Clinic, United States.

Robert and Arlene Kogod Center on Aging, Mayo Clinic, United States.

出版信息

Pharmacol Res. 2016 Sep;111:152-154. doi: 10.1016/j.phrs.2016.05.015. Epub 2016 May 27.

Abstract

Senescent cells accumulate in a variety of tissues with aging. They can develop a senescence-associated secretory phenotype (SASP) that entails secretion of inflammatory cytokines, chemokines, proteases, and growth factors. These SASP components can alter the microenvironment within tissues and affect the function of neighboring cells, which can eventually lead to local and systemic dysfunction. The JAK pathway is more highly activate in senescent than non-senescent cells. Inhibition of the JAK pathway suppresses the SASP in senescent cells and alleviates age-related tissue dysfunction. Targeting senescent cells could be a promising way to improve healthspan in aged population.

摘要

随着衰老,衰老细胞在多种组织中积累。它们会形成一种衰老相关分泌表型(SASP),这种表型会导致炎性细胞因子、趋化因子、蛋白酶和生长因子的分泌。这些SASP成分可改变组织内的微环境并影响邻近细胞的功能,最终可能导致局部和全身功能障碍。与非衰老细胞相比,JAK通路在衰老细胞中被更高度激活。抑制JAK通路可抑制衰老细胞中的SASP,并减轻与年龄相关的组织功能障碍。靶向衰老细胞可能是改善老年人群健康寿命的一种有前景的方法。

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