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线粒体功能障碍和衰老:多维机制和治疗策略

Pei Wei^1,2,3, Xiaoyan Zhang^1,2,3, Chi Yan^1,2,3,4

¹Department of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China.

|July 9, 2025

概括

细胞衰老驱动与年龄相关的疾病,线粒体功能障碍发挥着关键作用. 本综述探讨了新陈代谢变化,表观遗传学,端粒损伤,自和与衰老相关的分泌表型如何导致衰老和疾病.

科学领域:

老年学是一门学科.
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

衰老是一个复杂的过程,涉及到细胞和器官功能障碍.
全球预期寿命的增加凸显了了解衰老机制的迫切需要.
线粒体功能障碍是许多与年龄有关的疾病的中心病理因素.

研究的目的:

系统地审查将线粒体功能障碍与衰老联系起来的分子途径.
探索各种机制如何导致与年龄相关的细胞衰退和疾病.
确定延缓衰老和预防与年龄有关的疾病的潜在治疗点.

主要方法:

对推动衰老的分子途径进行系统审查.
分析包括代谢重编程,表观遗传调节和端粒损伤在内的机制.
检查自和老化相关分泌表型 (SASP) 的作用.

主要成果:

线粒体功能障碍通过代谢重编程 (例如PI3K/Akt/mTOR),表观遗传变化,端粒缩短 (p53-PGC-1α轴),自失衡和SASP驱动衰老.
赛尔图因 (SIRT1,SIRT3) 和其他因素调节线粒体平衡.
通过像cGAS-STING这样的途径调解的SASP促进炎症和疾病的进展.

结论:

线粒体功能障碍是衰老和与年龄有关的疾病的关键驱动因素.
针对sirtuins,AMPK,端粒酶,代谢重编程或SASP等途径提供了治疗潜力.
未来的研究应该整合多态学,并探索有机体相互作用,以进行精确的干预.

关键词:

衰老的衰老衰老的衰老自自是一种自的过程.表观遗传调节表观遗传调节代谢重编程是一种代谢重编程.线粒体中的线粒体.端粒功能障碍端粒功能障碍

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