ReviewTrends in genetics : TIG2024
Time is ticking faster for long genes in aging.
Review in Trends in genetics : TIG, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Consistent changes in global gene expression patterns despite strong variation in individual gene expression in the male mouse hippocampus following early life stress.Neurobiology of stress · 2026Article
- Poly(A)+ selection limits detection of long and alternatively spliced transcripts compared with rRNA depletion in RNA-Sequencing.BMC genomics · 2026Article
- The landscape of structural variation in pediatric cancer.Cancer cell · 2026Article
- Native entanglement misfolding contributes to age-associated structural changebioRxiv : the preprint server for biology · 2026Article
- Article
- Review
- Defective RNA processing and ELOA-mediated transcriptional elongation in reversible cellular senescence suggest aging by transcription.Molecular cell · 2025Article
- RNA dysfunction in age-related macular degeneration: the role of U1 snRNP complex and neurodegenerative diseases.International journal of retina and vitreous · 2025Review
- Targeting DNA damage in ageing: towards supercharging DNA repair.Nature reviews. Drug discovery · 2025Review
- Transcriptional Dysregulation of Autophagy in Aging and Potential Interventions: Insights Into TFEB and FOXOs.Frontiers in bioscience (Landmark edition) · 2025Review
- MYC: The Guardian of Its Own Chaos.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Article
- Article
- Article
- High protein intake causes gene-length-dependent transcriptional decline, shortens lifespan and accelerates ageing in progeroid DNA repair-deficient mice.npj metabolic health and disease · 2025Article
- Transcriptional stress in aging: integrating experimental data and modeling to quantify DNA damage accumulation.Frontiers in molecular biosciences · 2025Article
- Improved health by combining dietary restriction and promoting muscle growth in DNA repair-deficient progeroid mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- Optimal lifestyle patterns for delaying ageing and reducing all-cause mortality: insights from the UK Biobank.European review of aging and physical activity : official journal of the European Group for Research into Elderly and Physical Activity · 2024Article
- Gene length could be a critical factor in the aging of the genome.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 4 countries.
Funding
Abstract
Recent studies of aging organisms have identified a systematic phenomenon, characterized by a negative correlation between gene length and their expression in various cell types, species, and diseases. We term this phenomenon gene-length-dependent transcription decline (GLTD) and suggest that it may represent a bottleneck in the transcription machinery and thereby significantly contribute to aging as an etiological factor. We review potential links between GLTD and key aging processes such as DNA damage and explore their potential in identifying disease modification targets. Notably, in Alzheimer's disease, GLTD spotlights extremely long synaptic genes at chromosomal fragile sites (CFSs) and their vulnerability to postmitotic DNA damage. We suggest that GLTD is an integral element of biological aging.
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.