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衰老和抗衰老策略的分子机制。

Molecular mechanisms of aging and anti-aging strategies.

机构信息

Tianjin Institute of Industrial Biotechnology, Chinese Academy of Sciences; National Center of Technology Innovation for Synthetic Biology, Tianjin, China.

Institute of Life Sciences, Chongqing Medical University, Chongqing, China.

出版信息

Cell Commun Signal. 2024 May 24;22(1):285. doi: 10.1186/s12964-024-01663-1.

DOI:10.1186/s12964-024-01663-1
PMID:38790068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11118732/
Abstract

Aging is a complex and multifaceted process involving a variety of interrelated molecular mechanisms and cellular systems. Phenotypically, the biological aging process is accompanied by a gradual loss of cellular function and the systemic deterioration of multiple tissues, resulting in susceptibility to aging-related diseases. Emerging evidence suggests that aging is closely associated with telomere attrition, DNA damage, mitochondrial dysfunction, loss of nicotinamide adenine dinucleotide levels, impaired macro-autophagy, stem cell exhaustion, inflammation, loss of protein balance, deregulated nutrient sensing, altered intercellular communication, and dysbiosis. These age-related changes may be alleviated by intervention strategies, such as calorie restriction, improved sleep quality, enhanced physical activity, and targeted longevity genes. In this review, we summarise the key historical progress in the exploration of important causes of aging and anti-aging strategies in recent decades, which provides a basis for further understanding of the reversibility of aging phenotypes, the application prospect of synthetic biotechnology in anti-aging therapy is also prospected.

摘要

衰老是一个复杂而多方面的过程,涉及多种相互关联的分子机制和细胞系统。表型上,生物衰老过程伴随着细胞功能的逐渐丧失和多个组织的系统性恶化,导致易患与衰老相关的疾病。新出现的证据表明,衰老与端粒磨损、DNA 损伤、线粒体功能障碍、烟酰胺腺嘌呤二核苷酸水平降低、大自噬受损、干细胞衰竭、炎症、蛋白质平衡丧失、营养感应失调、细胞间通讯改变和微生态失调密切相关。这些与年龄相关的变化可以通过干预策略来缓解,如限制热量摄入、改善睡眠质量、增强体育锻炼和靶向长寿基因。在这篇综述中,我们总结了近几十年来探索衰老重要原因和抗衰老策略的关键历史进展,为进一步理解衰老表型的可逆性以及合成生物技术在抗衰老治疗中的应用前景提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/3f464f11838d/12964_2024_1663_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/4242ebc8d6b3/12964_2024_1663_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/61a0773680e4/12964_2024_1663_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/c084f4a840a7/12964_2024_1663_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/5299828a670f/12964_2024_1663_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/3f464f11838d/12964_2024_1663_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/4242ebc8d6b3/12964_2024_1663_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/5dbd9293c788/12964_2024_1663_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/61a0773680e4/12964_2024_1663_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/c084f4a840a7/12964_2024_1663_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/5299828a670f/12964_2024_1663_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/84ee/11118732/3f464f11838d/12964_2024_1663_Fig6_HTML.jpg

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