ArticleGenome research2019
Remodeling of epigenome and transcriptome landscapes with aging in mice reveals widespread induction of inflammatory responses.
Article in Genome research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers.
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243 citing papers in PubMed, 362 citations in OpenAlex.
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- Site-specific programming characterizes dynamic post-translational acetylation of histone H2B lysine 108 in mouse embryonic stem cells.Nature communications · 2026Article
- Integrated Genomic and Proteomic Analysis Reveals T-B Lymphocyte Signatures in the MYCN Driven "Immune Desert" of Specific Neuroblastoma Subtypes.CNS neuroscience & therapeutics · 2026Article
- Noncircadian BMAL1-YAP activity amplifies persistent inflammation in aged epidermis.Nature aging · 2026Article
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- Global StationaryOT: trajectory inference for aging time courses of single-cell snapshots.Bioinformatics (Oxford, England) · 2026Article
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- Tissue-resident colon macrophages shape the microbiome and regulate mucosal healing via ferroportin.Cell reports · 2026Article
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- An antagonistically pleiotropic gene regulates vertebrate growth, maturity, and lifespan.Nature communications · 2026Article
- A multi-omics analysis of human fibroblasts overexpressing an Alu transposon reveals widespread disruptions in aging-associated pathways.GeroScience · 2026Article
- Inhibition of salt-inducible kinases reprograms T cells and antitumor immunity in ovarian cancer.Nature immunology · 2026Article
- A dual role for cGAS in shaping cellular and organismal responses to genomic instability.Genes & development · 2026Article
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- HIRA-mediated H3.3 deposition preserves hepatocyte cell identity during liver aging.Research square · 2026Article
183 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Aging is accompanied by the functional decline of tissues. However, a systematic study of epigenomic and transcriptomic changes across tissues during aging is missing. Here, we generated chromatin maps and transcriptomes from four tissues and one cell type from young, middle-aged, and old mice-yielding 143 high-quality data sets. We focused on chromatin marks linked to gene expression regulation and cell identity: histone H3 trimethylation at lysine 4 (H3K4me3), a mark enriched at promoters, and histone H3 acetylation at lysine 27 (H3K27ac), a mark enriched at active enhancers. Epigenomic and transcriptomic landscapes could easily distinguish between ages, and machine-learning analysis showed that specific epigenomic states could predict transcriptional changes during aging. Analysis of data sets from all tissues identified recurrent age-related chromatin and transcriptional changes in key processes, including the up-regulation of immune system response pathways such as the interferon response. The up-regulation of the interferon response pathway with age was accompanied by increased transcription and chromatin remodeling at specific endogenous retroviral sequences. Pathways misregulated during mouse aging across tissues, notably innate immune pathways, were also misregulated with aging in other vertebrate species-African turquoise killifish, rat, and humans-indicating common signatures of age across species. To date, our data set represents the largest multitissue epigenomic and transcriptomic data set for vertebrate aging. This resource identifies chromatin and transcriptional states that are characteristic of young tissues, which could be leveraged to restore aspects of youthful functionality to old tissues.
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