Ji Zhejun, Liu Guang-Hui, Qu Jing
State Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
Beijing Institute for Stem Cell and Regenerative Medicine, Beijing 100101, China.
Life Med. 2025 Jun 9;4(4):lnaf019. doi: 10.1093/lifemedi/lnaf019. eCollection 2025 Aug.
Mitochondrial dysfunction is a hallmark of aging, characterized by a decline in mitochondrial biogenesis and quality control, compromised membrane integrity, elevated ROS production, damaged mitochondrial DNA (mtDNA), impaired mitochondrial-nuclear crosstalk, and deregulated metabolic balance. Among the key longevity regulators, sirtuin family members SIRT3, SIRT4, and SIRT5 are predominantly localized to mitochondria and play crucial roles in maintaining mitochondrial function and homeostasis. This review explores how mitochondrial sirtuins mitigate aging-related mitochondrial dysfunctions and their broader implications in aging-related diseases. By elucidating the intricate interplay between mitochondrial dysfunction and mitochondrial sirtuins, we aim to provide insights into therapeutic strategies for promoting healthy aging and combating age-related pathologies.
线粒体功能障碍是衰老的一个标志,其特征是线粒体生物合成和质量控制下降、膜完整性受损、活性氧生成增加、线粒体DNA(mtDNA)受损、线粒体-细胞核相互作用受损以及代谢平衡失调。在关键的长寿调节因子中,沉默调节蛋白家族成员SIRT3、SIRT4和SIRT5主要定位于线粒体,并在维持线粒体功能和稳态方面发挥关键作用。本综述探讨了线粒体沉默调节蛋白如何减轻与衰老相关的线粒体功能障碍及其在衰老相关疾病中的更广泛影响。通过阐明线粒体功能障碍与线粒体沉默调节蛋白之间的复杂相互作用,我们旨在为促进健康衰老和对抗与年龄相关的病理状况的治疗策略提供见解。