Previously, we uncovered a novel mechanism in which senescence is controlled by mitochondrial functional recovery upon Ataxia-telangiectasia mutated (ATM) inhibition. However, it remains elusive how ATM controls signaling pathways to achieve restorative effect. In this study, we performed microarray and found that p53 pathway was differentially expressed upon ATM inhibition. We found that ATM inhibition yields senescence amelioration through p53-dependent manner. The restorative effect was also afforded by direct p53 inhibition. Furthermore, mitochondrial metabolic reprogramming via p53 inhibition was a prerequisite for senescence amelioration. Taken together, our data indicated that p53 pathway functions as potential target for ATM-mediated senescence amelioration.

中文翻译：

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ATM 介导的 p53 信号通路形成衰老控制的新轴

以前，我们发现了一种新机制，其中衰老是由线粒体功能恢复控制的共济失调毛细血管扩张突变 (ATM) 抑制。然而，ATM 如何控制信号通路以实现恢复作用仍然难以捉摸。在这项研究中，我们进行了微阵列，发现 p53 通路在 ATM 抑制后差异表达。我们发现 ATM 抑制通过 p53 依赖性方式产生衰老改善。直接抑制 p53 也提供了恢复作用。此外，通过 p53 抑制进行的线粒体代谢重编程是衰老改善的先决条件。总之，我们的数据表明 p53 途径作为 ATM 介导的衰老改善的潜在目标。