ReviewAging cell2017
The emerging role of alternative splicing in senescence and aging.
Review in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
What it found
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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.
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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.
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Who cites it
107 citing papers in PubMed.
- A Hypertrophic Stimulus Drives Age-Dependent Transcript Isoform Switching With and Without Differential Gene Expression in Skeletal Muscle.Aging cell · 2026Article
- Alternative Splicing Constitutes a Transcription-independent Regulatory Layer in Replicative Senescence of Human Umbilical Cord Mesenchymal Stem Cells.Stem cell reviews and reports · 2026Article
- Single-cell splice isoform usage reveals distinct axes of cellular identity and senescence.bioRxiv : the preprint server for biology · 2026Article
- Mammalian aging involves genome-wide splicing degeneration leading to functional decline.bioRxiv : the preprint server for biology · 2026Article
- RNA-Binding Proteins in Ageing and Age-Related Disease.Neurology international · 2026Review
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- The aging genome exhibits organized vulnerability to somatic mutations.bioRxiv : the preprint server for biology · 2026Article
- Locus-specific LINE-1 mRNA expression reflects cell-type- and stimulus-specific senescence states.Nucleic acids research · 2026Article
- An snRNA-seq aging clock for the fruit fly head sheds light on sex-biased aging.Scientific reports · 2026Article
- Tabula Sapiens reveals the non-coding RNA landscape across 22 human organs and tissues.bioRxiv : the preprint server for biology · 2026Article
- Using RNA-targeting CRISPR-Cas13 and engineered U1 systems to targetMolecular therapy. Nucleic acids · 2026Article
- Article
- Beyond a gatekeeper: the non-classical signaling role of STRA6 in driving endothelial senescence and atherosclerosis.Frontiers in immunology · 2026Review
- Characterization of the Intact Proteomic Profile of Senescent-Associated Secretory Phenotype by Top-Down Mass Spectrometry.Analytical chemistry · 2025Article
- RNA dysfunction in age-related macular degeneration: the role of U1 snRNP complex and neurodegenerative diseases.International journal of retina and vitreous · 2025Review
- Assessing tissue-specific gene expression of essential genes from human and mouse.Briefings in bioinformatics · 2025Article
- Altered translation elongation contributes to key hallmarks of aging in the killifish brain.Science (New York, N.Y.) · 2025Article
- Retained introns in phototransduction genes of 5xFAD mouse retina suggest vision impairment as an early diagnostic marker for Alzheimer's disease.Scientific reports · 2025Article
- Therapy-induced senescence is a transient drug resistance mechanism in breast cancer.Molecular cancer · 2025Article
- Splicing accuracy varies across human introns, tissues, age and disease.Nature communications · 2025Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deregulation of precursor mRNA splicing is associated with many illnesses and has been linked to age-related chronic diseases. Here we review recent progress documenting how defects in the machinery that performs intron removal and controls splice site selection contribute to cellular senescence and organismal aging. We discuss the functional association linking p53, IGF-1, SIRT1, and ING-1 splice variants with senescence and aging, and review a selection of splicing defects occurring in accelerated aging (progeria), vascular aging, and Alzheimer's disease. Overall, it is becoming increasingly clear that changes in the activity of splicing factors and in the production of key splice variants can impact cellular senescence and the aging phenotype.
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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.