Levine Morgan E, Lu Ake T, Quach Austin, Chen Brian H, Assimes Themistocles L, Bandinelli Stefania, Hou Lifang, Baccarelli Andrea A, Stewart James D, Li Yun, Whitsel Eric A, Wilson James G, Reiner Alex P, Aviv Abraham, Lohman Kurt, Liu Yongmei, Ferrucci Luigi, Horvath Steve
Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.
Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, USA, Baltimore, MD 21224, USA.
Aging (Albany NY). 2018 Apr 18;10(4):573-591. doi: 10.18632/aging.101414.
Identifying reliable biomarkers of aging is a major goal in geroscience. While the first generation of epigenetic biomarkers of aging were developed using chronological age as a surrogate for biological age, we hypothesized that incorporation of composite clinical measures of phenotypic age that capture differences in lifespan and healthspan may identify novel CpGs and facilitate the development of a more powerful epigenetic biomarker of aging. Using an innovative two-step process, we develop a new epigenetic biomarker of aging, DNAm PhenoAge, that strongly outperforms previous measures in regards to predictions for a variety of aging outcomes, including all-cause mortality, cancers, healthspan, physical functioning, and Alzheimer's disease. While this biomarker was developed using data from whole blood, it correlates strongly with age in every tissue and cell tested. Based on an in-depth transcriptional analysis in sorted cells, we find that increased epigenetic, relative to chronological age, is associated with increased activation of pro-inflammatory and interferon pathways, and decreased activation of transcriptional/translational machinery, DNA damage response, and mitochondrial signatures. Overall, this single epigenetic biomarker of aging is able to capture risks for an array of diverse outcomes across multiple tissues and cells, and provide insight into important pathways in aging.
识别可靠的衰老生物标志物是老年科学的一个主要目标。虽然第一代衰老表观遗传生物标志物是使用实际年龄作为生物学年龄的替代指标来开发的,但我们推测,纳入能够反映寿命和健康跨度差异的表型年龄综合临床指标,可能会识别出新的CpG位点,并有助于开发出更强大的衰老表观遗传生物标志物。通过一个创新的两步法,我们开发了一种新的衰老表观遗传生物标志物——DNA甲基化表型年龄(DNAm PhenoAge),在预测各种衰老结果方面,包括全因死亡率、癌症、健康跨度、身体功能和阿尔茨海默病,它的表现远远优于以往的指标。虽然这种生物标志物是使用全血数据开发的,但它与所测试的每个组织和细胞中的年龄都有很强的相关性。基于对分选细胞的深入转录分析,我们发现,相对于实际年龄,表观遗传增加与促炎和干扰素通路的激活增加有关,而与转录/翻译机制、DNA损伤反应和线粒体特征的激活减少有关。总体而言,这种单一的衰老表观遗传生物标志物能够捕捉多个组织和细胞中一系列不同结果的风险,并深入了解衰老过程中的重要通路。