时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, although aging is widely recognized as a risk factor for disease, whether and how disease states deviate from, accelerate, or transiently reshape healthy aging trajectories remains insufficiently characterized in a systematic and quantitative manner [, , ].；Yet it remains unclear whether COVID-19-associated transcriptomic alterations can be quantitatively positioned relative to healthy aging trajectories at the individual level.；However, different omics-based clocks capture distinct layers of aging biology.
方法
In total, 23 publicly available cohorts were collected, including GSE203024, GSE97531, GSE140829, GSE221615, GSE141661, GSE124326, GSE51216, GSE193771, GSE158699, GSE177044, GSE111368, GSE61821, GSE185576, GSE146446, GSE98793, GSE152641, GSE161731, GSE228839, GSE231409, GSE185263, GSE66175, GSE169687, and GSE198449.；Among these, nine datasets (GSE203024, GSE97531, GSE140829, GSE221615, GSE141661, GSE124326, GSE51216, GSE193771, and GSE158699) were designated as internal cohorts for model development.；GSE177044 was used as an external tuning cohort for model selection and hyperparameter optimization.；In addition, four datasets (GSE185263, GSE66175, GSE169687, and GSE198449) were reserved as independent external cohorts for downstream prediction and exploratory analyses.
核心结论
Using a significance threshold of false discovery rate (FDR) < 0.05, we identified 2977 genes whose expression decreased with age and 1609 genes whose expression increased with age ().；Genes upregulated during aging were predominantly enriched in pathways related to innate immune response, type I interferon signaling, NF-κB signaling, and coagulation, whereas age-downregulated genes were mainly associated with RNA processing, ribonucleoprotein complex biogenesis, mitochondrial gene expression, and chromatin organization ().；Collectively, these findings indicate that COVID-19 and aging share partially overlapping transcriptomic functional signatures in peripheral blood, particularly characterized by enhanced innate immunity, interferon responses, and inflammatory processes [, ]. ‖ 结论：These findings suggest that COVID-19 does not simply activate isolated antiviral pathways, but induces a broader remodeling of blood molecular homeostasis that partially converges with aging-associated programs.
局限
By constructing a BAP from healthy individuals, our study reframes transcriptomic AgeAccel from a conventional residual of age prediction into an interpretable measure of how far an individual’s molecular state deviates from the expected trajectory of healthy aging.；Therefore, this analysis reflects group-level changes rather than within-subject residual effects of COVID-19.；An important limitation is that the current BAP framework relies on cohort-level normalization and batch correction and was therefore not designed for direct application to a single new sample in the absence of appropriate reference data.
对本项目的价值
★☆☆☆☆ 炎症衰老是几乎所有慢性老年病的公共通路，也是最有希望做「抗炎但保留免疫」解耦的靶点。
全文来源
PMC JATS 全文（正文 53,115 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：A blood aging clock defines disease-induced deviation from healthy molecular aging.
- 期刊与标识：Brief Bioinform · PMID 42960996 · DOI 10.1093/bib/bbag605
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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