研究动态
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肺部表观遗传年龄、炎症和基因表达加速:吸烟者和电子烟使用者与非吸烟者的比较。

Accelerated epigenetic age, inflammation, and gene expression in lung: comparisons of smokers and vapers with non-smokers.

发表日期:2023 Oct 11
作者: Min-Ae Song, Kellie M Mori, Joseph P McElroy, Jo L Freudenheim, Daniel Y Weng, Sarah A Reisinger, Theodore M Brasky, Mark D Wewers, Peter G Shields
来源: Clinical Epigenetics

摘要:

吸烟和衰老是肺部疾病(包括癌症)的主要危险因素。表观遗传衰老可以解释吸烟、电子烟和肺部健康之间的关系。尚无研究检查吸烟和电子烟相关的表观遗传衰老与肺部生物标志物的关系。通过 DNA 甲基化 (mAge) 及其加速 (mAA) 测量的肺表观遗传衰老在年轻(21-30 岁)电子烟吸烟者中进行了评估(EC,n) = 14,其中包括 3 名从不吸烟的 EC)、吸烟者(SM,n = 16)和非 EC/非 SM(NS,n = 39)。我们研究了 mAge 估计值与实际年龄 (Horvath-mAge)、寿命/死亡率 (Grim-mAge)、端粒长度 (TL-mAge)、吸烟/EC 史、尿生物标志物、肺细胞因子和转录组的关系。与 NS 相比, EC和SM的Grim-mAge显着变老,TL-mAge变短,Grim-mAge显着加速,TL-mAge显着减速。在 SM 中,Grim-mAA 与尼古丁摄入量和 4-(甲基亚硝基氨基)-1-(3-吡啶基)-1-丁醇 (NNAL) 相关。对于 EC,Horvath-mAA 与每天的抽吸次数显着相关。总体而言,细胞因子(IL-1β、IL-6 和 IL-8)和 759 个转录物(651 个独特基因)与 Grim-mAA 显着相关。 Grim-mAA 相关基因在免疫相关途径和在细胞/组织的形态和结构中发挥作用的基因中高度富集。SM 的更快的肺 mAge 与先前的血液研究一致。与 NS 相比,EC 的肺 mage 更快,表明 EC 对生物衰老可能产生不利的肺部影响。我们的研究结果支持进一步研究,特别是关于表观遗传标记、吸烟和电子烟对肺部健康影响的研究。鉴于大多数 EC 都是前吸烟者,需要进一步研究以了解电子烟对生物衰老的独特影响。© 2023。BioMed Central Ltd.,Springer Nature 旗下公司。
Cigarette smoking and aging are the main risk factors for pulmonary diseases, including cancer. Epigenetic aging may explain the relationship between smoking, electronic cigarette vaping, and pulmonary health. No study has examined smoking and vaping-related epigenetic aging in relation to lung biomarkers.Lung epigenetic aging measured by DNA methylation (mAge) and its acceleration (mAA) was assessed in young (age 21-30) electronic cigarette vapers (EC, n = 14, including 3 never-smoking EC), smokers (SM, n = 16), and non-EC/non-SM (NS, n = 39). We investigated relationships of mAge estimates with chronological age (Horvath-mAge), lifespan/mortality (Grim-mAge), telomere length (TL-mAge), smoking/EC history, urinary biomarkers, lung cytokines, and transcriptome.Compared to NS, EC and SM had significantly older Grim-mAge, shorter TL-mAge, significantly accelerated Grim-mAge and decelerated TL-mAge. Among SM, Grim-mAA was associated with nicotine intake and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL). For EC, Horvath-mAA was significantly correlated with puffs per day. Overall, cytokines (IL-1β, IL-6, and IL-8) and 759 transcripts (651 unique genes) were significantly associated with Grim-mAA. Grim-mAA-associated genes were highly enriched in immune-related pathways and genes that play a role in the morphology and structures of cells/tissues.Faster lung mAge for SM is consistent with prior studies of blood. Faster lung mAge for EC compared to NS indicates possible adverse pulmonary effects of EC on biological aging. Our findings support further research, particularly on epigenetic markers, on effects of smoking and vaping on pulmonary health. Given that most EC are former smokers, further study is needed to understand unique effects of electronic cigarettes on biological aging.© 2023. BioMed Central Ltd., part of Springer Nature.