ArticleNature communications2023
Multi-omic underpinnings of epigenetic aging and human longevity.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed.
- Speech clocks decode dementia phenotypes, social exposome, and biological aging.Science advances · 2026Article
- Metabolic Profiling of Epigenetic Aging and Its Associations With Aging-Related Phenotypes and Modifiable Lifestyle Factors.Aging cell · 2026Article
- Biological Aging, Immune Phenotypes, and Susceptibility to COVID-19 and Sepsis: A Mendelian Randomization Study.Virus research · 2026Article
- Association of biological age acceleration with muscle aging phenotype in young and middle-aged adults: a prospective cohort study.GeroScience · 2026Article
- DNA methylation clock in bull sperm cells reveals the epigenetic aging characteristics and impact on fertility.Journal of animal science and biotechnology · 2026Article
- The Evolving Landscape of Clinical Aging Clocks: From Epigenetic to Multi-Omics Integration.Aging cell · 2026Review
- Decoding disease and therapy through multiomics integration and systems analysis.Briefings in bioinformatics · 2026Review
- Oridonin as a novel KDM5C inhibitor alleviates clonal hematopoiesis-induced cardiac agingActa pharmaceutica Sinica. B · 2026Article
- Iron status modulates immune cell proportions to drive epigenetic age acceleration: A 2-step Mendelian randomization study.Medicine · 2026Article
- Recommendations for biomarker data collection in clinical trials by longevity biotechnology companies.npj aging · 2025Article
- Causal effects of immune cell populations on biological aging: a Mendelian randomization study.Biogerontology · 2025Article
- Proteome atlas for mechanistic discovery and risk prediction of diabetic retinopathy.Nature communications · 2025Article
- Mendelian randomization study implicates inflammaging biomarkers in retinal vasculature, cardiovascular diseases, and longevity.Science advances · 2025Article
- Metabolomic-based aging clocks.npj metabolic health and disease · 2025Review
- Refining the generation, interpretation and application of multi-organ, multi-omics biological aging clocks.Nature aging · 2025Article
- Epigenetic Clocks Identify Harmful Epigenetic Aging Linked to Depression Severity and Cognitive Deficits in Major Depressive Disorder.Aging and disease · 2025Article
- Multi-Omic Associations of Epigenetic Age Acceleration Are Heterogeneously Shaped by Genetic and Environmental Influences.Aging cell · 2025Article
- Epigenetic clocks as mediators of health behaviors and mortality in middle-aged and older adults.The journal of nutrition, health & aging · 2025Article
- Systematic druggable genome-wide Mendelian randomization identifies therapeutic targets for osteoporosis.Osteoporosis and sarcopenia · 2025Article
- Genetic determinants of proteomic aging.npj aging · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Biological aging is accompanied by increasing morbidity, mortality, and healthcare costs; however, its molecular mechanisms are poorly understood. Here, we use multi-omic methods to integrate genomic, transcriptomic, and metabolomic data and identify biological associations with four measures of epigenetic age acceleration and a human longevity phenotype comprising healthspan, lifespan, and exceptional longevity (multivariate longevity). Using transcriptomic imputation, fine-mapping, and conditional analysis, we identify 22 high confidence associations with epigenetic age acceleration and seven with multivariate longevity. FLOT1, KPNA4, and TMX2 are novel, high confidence genes associated with epigenetic age acceleration. In parallel, cis-instrument Mendelian randomization of the druggable genome associates TPMT and NHLRC1 with epigenetic aging, supporting transcriptomic imputation findings. Metabolomics Mendelian randomization identifies a negative effect of non-high-density lipoprotein cholesterol and associated lipoproteins on multivariate longevity, but not epigenetic age acceleration. Finally, cell-type enrichment analysis implicates immune cells and precursors in epigenetic age acceleration and, more modestly, multivariate longevity. Follow-up Mendelian randomization of immune cell traits suggests lymphocyte subpopulations and lymphocytic surface molecules affect multivariate longevity and epigenetic age acceleration. Our results highlight druggable targets and biological pathways involved in aging and facilitate multi-omic comparisons of epigenetic clocks and human longevity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.