衰老标志的因果关系。

IF 6.9 2区医学 Q1 GERIATRICS & GERONTOLOGY

Aging and Disease Pub Date : 2025-05-20 DOI:10.14336/AD.2025.0541

Bilu Huang, Xiaowen Hu

{"title":"衰老标志的因果关系。","authors":"Bilu Huang, Xiaowen Hu","doi":"10.14336/AD.2025.0541","DOIUrl":null,"url":null,"abstract":"This article emphasizes the causal relationship in the mechanisms of aging, asserting that among the twelve hallmarks of aging, only telomere shortening is the cause of aging. The \"Telomere DNA and ribosomal DNA co-regulation model for cell senescence\" suggests that the shortening of telomeres and rDNA arrays can mediate various hallmarks of aging through the P53 pathway. Therefore, the best way to reverse aging and significantly extend lifespan is to increase the length of telomeres and rDNA arrays in adult stem cells within tissues.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":6.9000,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Causality of Aging Hallmarks.\",\"authors\":\"Bilu Huang, Xiaowen Hu\",\"doi\":\"10.14336/AD.2025.0541\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This article emphasizes the causal relationship in the mechanisms of aging, asserting that among the twelve hallmarks of aging, only telomere shortening is the cause of aging. The \\\"Telomere DNA and ribosomal DNA co-regulation model for cell senescence\\\" suggests that the shortening of telomeres and rDNA arrays can mediate various hallmarks of aging through the P53 pathway. Therefore, the best way to reverse aging and significantly extend lifespan is to increase the length of telomeres and rDNA arrays in adult stem cells within tissues.\",\"PeriodicalId\":7434,\"journal\":{\"name\":\"Aging and Disease\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":6.9000,\"publicationDate\":\"2025-05-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Aging and Disease\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.14336/AD.2025.0541\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"GERIATRICS & GERONTOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Aging and Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.14336/AD.2025.0541","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}

引用次数: 0

摘要

本文强调衰老机制中的因果关系，认为在衰老的十二个标志中，只有端粒缩短是导致衰老的原因。“端粒DNA和核糖体DNA共同调控细胞衰老模型”表明，端粒和rDNA阵列的缩短可以通过P53通路介导各种衰老标志。因此，逆转衰老和显著延长寿命的最佳途径是增加组织内成体干细胞端粒和rDNA阵列的长度。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

Causality of Aging Hallmarks.

This article emphasizes the causal relationship in the mechanisms of aging, asserting that among the twelve hallmarks of aging, only telomere shortening is the cause of aging. The "Telomere DNA and ribosomal DNA co-regulation model for cell senescence" suggests that the shortening of telomeres and rDNA arrays can mediate various hallmarks of aging through the P53 pathway. Therefore, the best way to reverse aging and significantly extend lifespan is to increase the length of telomeres and rDNA arrays in adult stem cells within tissues.

求助全文

通过发布文献求助，成功后即可免费获取论文全文。去求助

来源期刊

Aging and Disease GERIATRICS & GERONTOLOGY-

CiteScore

14.60

自引率

2.70%

发文量

138

审稿时长

10 weeks

期刊介绍： Aging & Disease (A&D) is an open-access online journal dedicated to publishing groundbreaking research on the biology of aging, the pathophysiology of age-related diseases, and innovative therapies for conditions affecting the elderly. The scope encompasses various diseases such as Stroke, Alzheimer's disease, Parkinson’s disease, Epilepsy, Dementia, Depression, Cardiovascular Disease, Cancer, Arthritis, Cataract, Osteoporosis, Diabetes, and Hypertension. The journal welcomes studies involving animal models as well as human tissues or cells.