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衰老相关的关键信号通路及健康衰老的潜在干预靶点

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging.

机构信息

Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, China.

Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

出版信息

Cells. 2021 Mar 16;10(3):660. doi: 10.3390/cells10030660.

DOI:10.3390/cells10030660
PMID:33809718
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8002281/
Abstract

Aging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.

摘要

衰老是一个伴随着组织功能普遍下降的基本生物学过程。事实上,随着寿命的延长,与年龄相关的功能障碍,如认知障碍或痴呆,将成为一个日益严重的公共卫生问题。衰老是许多与年龄相关疾病的一个重要危险因素。如今,人们不仅希望活得更久,而且更健康。因此,我们迫切需要了解调节衰老的细胞和分子机制,这将使我们能够改变衰老过程,实现健康衰老,并减轻与年龄相关的疾病。在这里,我们回顾了对生物衰老的机制理解的最新突破,重点介绍了目前被认为对衰老至关重要的腺苷一磷酸激活的蛋白激酶 (AMPK)、Sirtuin 1 (SIRT1) 和雷帕霉素哺乳动物靶蛋白 (mTOR) 途径。我们还讨论了这些蛋白质和途径如何可能相互作用调节衰老。我们进一步描述了这些途径的知识如何可能导致新的抗衰老和对抗与年龄相关疾病的干预措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/76b85a3f4c95/cells-10-00660-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/ed55e93c6331/cells-10-00660-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/0b38918d1ab3/cells-10-00660-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/1fd3ba917fdf/cells-10-00660-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/76b85a3f4c95/cells-10-00660-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/ed55e93c6331/cells-10-00660-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/0b38918d1ab3/cells-10-00660-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/1fd3ba917fdf/cells-10-00660-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e375/8002281/76b85a3f4c95/cells-10-00660-g004.jpg

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