Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Tianjin Medical University, Tianjin, 300070, China.
Biogerontology. 2019 Feb;20(1):1-16. doi: 10.1007/s10522-018-9769-1. Epub 2018 Sep 18.
Aging is a biological process characterized by a progressive functional decline in tissues and organs, which eventually leads to mortality. Telomeres, the repetitive DNA repeat sequences at the end of linear eukaryotic chromosomes protecting chromosome ends from degradation and illegitimate recombination, play a crucial role in cell fate and aging. Due to the mechanism of replication, telomeres shorten as cells proliferate, which consequently contributes to cellular senescence and mitochondrial dysfunction. Cells are the basic unit of organismal structure and function, and mitochondria are the powerhouse and metabolic center of cells. Therefore, cellular senescence and mitochondrial dysfunction would result in tissue or organ degeneration and dysfunction followed by somatic aging through multiple pathways. In this review, we summarized the main mechanisms of cellular senescence, mitochondrial malfunction and aging triggered by telomere attrition. Understanding the molecular mechanisms involved in the aging process may elicit new strategies for improving health and extending lifespan.
衰老是一个生物学过程,其特征是组织和器官的功能逐渐下降,最终导致死亡。端粒是线性真核染色体末端保护染色体末端免受降解和非同源重组的重复 DNA 重复序列,在细胞命运和衰老中起着至关重要的作用。由于复制机制,随着细胞的增殖,端粒会缩短,这导致细胞衰老和线粒体功能障碍。细胞是生物体结构和功能的基本单位,线粒体是细胞的动力和代谢中心。因此,通过多种途径,细胞衰老和线粒体功能障碍会导致组织或器官退化和功能障碍,进而导致躯体衰老。在这篇综述中,我们总结了端粒磨损引发的细胞衰老、线粒体功能障碍和衰老的主要机制。了解衰老过程中涉及的分子机制可能会引发改善健康和延长寿命的新策略。