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早年接触烟草、遗传易感性与成年期生物衰老加速

Early-life exposure to tobacco, genetic susceptibility, and accelerated biological aging in adulthood.

作者信息

Cui Feipeng, Tang Linxi, Li Dankang, Ma Yudiyang, Wang Jianing, Xie Junqing, Su Binbin, Tian Yaohua, Zheng Xiaoying

机构信息

Key Laboratory of Environment and Health, Ministry of Education & Ministry of Environmental Protection, and State Key Laboratory of Environmental Health (incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, PR China.

Department of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, No. 13 Hangkong Road, Wuhan 430030, Hubei, PR China.

出版信息

Sci Adv. 2024 May 3;10(18):eadl3747. doi: 10.1126/sciadv.adl3747.

DOI:10.1126/sciadv.adl3747
PMID:38701212
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11068008/
Abstract

Early-life tobacco exposure serves as a non-negligible risk factor for aging-related diseases. To understand the underlying mechanisms, we explored the associations of early-life tobacco exposure with accelerated biological aging and further assessed the joint effects of tobacco exposure and genetic susceptibility. Compared with those without in utero exposure, participants with in utero tobacco exposure had an increase in Klemera-Doubal biological age (KDM-BA) and PhenoAge acceleration of 0.26 and 0.49 years, respectively, but a decrease in telomere length of 5.34% among 276,259 participants. We also found significant dose-response associations between the age of smoking initiation and accelerated biological aging. Furthermore, the joint effects revealed that high-polygenic risk score participants with in utero exposure and smoking initiation in childhood had the highest accelerated biological aging. There were interactions between early-life tobacco exposure and age, sex, deprivation, and diet on KDM-BA and PhenoAge acceleration. These findings highlight the importance of reducing early-life tobacco exposure to improve healthy aging.

摘要

早年接触烟草是与衰老相关疾病不可忽视的危险因素。为了解其潜在机制,我们探讨了早年接触烟草与生物衰老加速之间的关联,并进一步评估了烟草接触与遗传易感性的联合作用。在276,259名参与者中,与未在子宫内接触烟草的人相比,子宫内接触烟草的参与者的克莱梅拉-杜巴尔生物年龄(KDM-BA)增加了0.26岁,表型年龄加速增加了0.49岁,但端粒长度减少了5.34%。我们还发现开始吸烟的年龄与生物衰老加速之间存在显著的剂量反应关系。此外,联合作用表明,子宫内接触烟草且童年开始吸烟的高多基因风险评分参与者的生物衰老加速程度最高。早年接触烟草与年龄、性别、贫困和饮食在KDM-BA和表型年龄加速方面存在相互作用。这些发现凸显了减少早年接触烟草对促进健康衰老的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/67113b5218ef/sciadv.adl3747-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/804e03f9ee5a/sciadv.adl3747-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/2f25dd90d1d5/sciadv.adl3747-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/67113b5218ef/sciadv.adl3747-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/804e03f9ee5a/sciadv.adl3747-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/2f25dd90d1d5/sciadv.adl3747-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3f28/11068008/67113b5218ef/sciadv.adl3747-f3.jpg

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