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Nature Commun:衰老问题重要线索----转录因子调控细胞自噬

2017-10-16 欧阳沐 生物通

凯斯西储大学医学院和大学健康系统医院的研究人员发现了一个控制线虫和哺乳动物寿命的新分子通路。文章发表在今天的《Nature Communications》。


凯斯西储大学医学院和大学健康系统医院的研究人员发现了一个控制线虫和哺乳动物寿命的新分子通路。文章发表在近日的《Nature Communications》。

研究人员表示,某些蛋白质含量过高的线虫,比正常线虫寿命更长、活得更健康。这些蛋白含量过高的小鼠模型表现为延迟出现衰老相关的血管功能障碍。这项研究对了解衰老和衰老相关疾病有重要意义。

“我们发现,人为增加或减少KLFs(Kruppel样转录因子)蛋白家族水平,可以控制线虫寿命长短,”文章一作Nelson Hsieh MD/PHD说。“由于哺乳动物也存在同样的蛋白质家族,真正令人兴奋的是,我们的数据表明,KLFs对哺乳动物衰老也具有类似的调控效果。”

“许多衰老相关疾病,如高血压、心脏病、老年痴呆都与血管功能有关,我们观察到随着年龄增长KLF水平降低。相反,维持KLFs水平可预防衰老相关的血管功能损伤,”通讯作者、医学院副院长、附属医院首席科学官Mukesh K. Jain教授补充道。

进一步调查,研究人员发现KLF蛋白通过管理自噬(autophag)行使作用。这种高质量的控制机制一旦丧失就会出现老化标志。

“随着细胞年龄增长,自噬控制能力随即下降,”作者解释。“这可能会导致有毒蛋白质的持续聚集,最终妨碍细胞生存。缺乏KLF蛋白,线虫的自噬就无法维持,导致线虫过早死亡。”
突破性进展:抑制自噬,重返青春

研究人员表示,下一步研究将会探讨血管内壁细胞自噬如何改善血管功能的确切机制,他们还在寻求研究人类KLF蛋白的具体策略。“随着人口老龄化,在生命后期人类赖以生存的心脏和动脉如何继续顺畅工作?如何设计减缓心血管系统功能性老化的干预措施?这些都是我们未来要解决的问题。”

原始出处:

Paishiun N. Hsieh, Guangjin Zhou, Yiyuan Yuan,et al.A conserved KLF-autophagy pathway modulates nematode lifespan and mammalian age-associated vascular dysfunction.Nature Communications 8, Article number: 914 (2017)doi:10.1038/s41467-017-00899-5

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    2018-05-14 mjldent
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    2017-10-30 liuli5079
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    2018-03-05 liye789132251
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