Transcriptional Signatures of Aging
Open accessAbstract
Genome-wide studies of aging have identified subsets of genes that show age-related changes in expression. Although the types of genes that are age regulated vary among different tissues and organisms, some patterns emerge from these large data sets. First, aging is associated with a broad induction of stress response pathways, although the specific genes and pathways involved differ depending on cell type and species. In contrast, a wide variety of functional classes of genes are downregulated with age, often including tissue-specific genes. Although the upregulation of age-regulated genes is likely to be governed by stress-responsive transcription factors, questions remain as to why particular genes are susceptible to age-related transcriptional decline. Here, we discuss recent findings showing that splicing is misregulated with age. While defects in splicing could lead to changes in protein isoform levels, they could also impact gene expression through nonsense-mediated decay of intron-retained transcripts. The discovery that splicing is misregulated with age suggests that other aspects of gene expression, such as transcription elongation, termination, and polyadenylation, must also be considered as potential mechanisms for age-related changes in transcript levels. Moreover, the considerable variation between genome-wide aging expression studies indicates that there is a critical need to analyze the transcriptional signatures of aging in single-cell types rather than whole tissues. Since age-associated decreases in gene expression could contribute to a progressive decline in cellular function, understanding the mechanisms that determine the aging transcriptome provides a potential target to extend healthy cellular lifespan.
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We detected upregulation of complement, interferon and TNF/NF-κB pathways in senescent cells, which are robustly activated with ageing across vertebrate tissues, including humans.
“We detected upregulation of complement, interferon and TNF/NF-κB pathways in senescent cells, which are robustly activated with ageing across vertebrate tissues, including humans36–38.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [37]
The section ‘What types of genes show age-associated changes in expression?’ reports reproducible age-related upregulation of immune-response genes across species and tissues, including in humans, and implicates NF-κB in age-related changes. It does not establish that complement, interferon, and TNF/NF-κB pathways specifically are all robustly activated with age across vertebrate tissues. The senescent-cell detection is the citing authors’ own finding, not a finding attributed to this source. (LLM, conf=0.86)
Experimental — accuracy not yet measuredComparison of transcriptomes of ageing tissues from various species (including humans) with those of Sen cells from injured young muscles found an increase in inflammatory pathways (interferon, complement and cytokine and TNF/NF-κB signalling), consistent with previously published datasets.
“We next compared the transcriptomes of ageing tissues from various species (including humans) with those of Sen cells from injured young muscles, and found an increase in inflammatory pathways (interferon, complement and cytokine and TNF/NF-κB signalling) (Fig. 5b), consistent with previously published datasets36–38.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [37]
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Coefficient of variation of lifespan across the tree of life: Is it a signature of programmed aging?
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Age-associated bimodal transcriptional drift reduces intergenic disparities in transcription
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Aging, Life History, and Human Evolution
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- Authors
- Stegeman, R., & Weake, V. M.
- Affiliations
- Purdue University West Lafayette (US)
- Corresponding author
- Weake, V.M.
- Venue
- Journal of Molecular Biology
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 429
- Issue
- 16
- Pages
- 2427-2437
- ISSN
- 0022-2836 (ISSN-L)
- PMC
- PMC5662117
- OpenAlex
- W2730425696
- Cited by
- 146
- References
- 106
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 16 · 2023: 28 · 2022: 25 · 2021: 19 · 2020: 23 · 2019: 7 · 2018: 7 · 2017: 4
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Journal of Molecular Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (R01EY024905)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- aging, age-related gene expression, gene expression signatures, stress response pathways, transcription factors, nonsense-mediated mRNA decay, protein isoforms, transcription elongation, polyadenylation, tissue-specific genes, single-cell analysis, cellular lifespan
- MeSH terms
- Aging, Animals, Gene Expression Regulation, Humans, RNA Splicing, Protein Isoforms, Gene Expression Profiling
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