ReviewMechanisms of ageing and development2010
A LINE-1 component to human aging: do LINE elements exact a longevity cost for evolutionary advantage?
Review in Mechanisms of ageing and development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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
37 citing papers in PubMed, 65 citations in OpenAlex.
- Variation in LINE-1 ORF1p expression across histologic and demographic subgroups in non-small cell lung cancers.Translational oncology · 2026Article
- An FDA-Approved Tenofovir Alafenamide-Based Antiretroviral Therapy Reduces Biological Age in Healthy Adults: First Human Proof-of-Concept for Retrotransposon-Targeted Gerotherapeutics.medRxiv : the preprint server for health sciences · 2026Article
- MORE-RNAseq: a pipeline for quantifying retrotransposition-capable LINE1 expression based on RNA-seq data.Frontiers in bioinformatics · 2025Article
- LINE-1 retrotransposon activation drives age-associated inflammationContemporary oncology (Poznan, Poland) · 2025Review
- Repetitive Sequence Stability in Embryonic Stem Cells.International journal of molecular sciences · 2024Review
- Therapeutic value of homeoprotein signaling pathways.Frontiers in neuroscience · 2024Review
- Navigating the brain and aging: exploring the impact of transposable elements from health to disease.Frontiers in cell and developmental biology · 2024Review
- The Ultraviolet Irradiation of Keratinocytes Induces Ectopic Expression of LINE-1 Retrotransposon Machinery and Leads to Cellular Senescence.Biomedicines · 2023Article
- Aryl hydrocarbon receptor (AhR) reveals evidence of antagonistic pleiotropy in the regulation of the aging process.Cellular and molecular life sciences : CMLS · 2022Review
- Patients with Lung Cancer of Different Racial Backgrounds Harbor Distinct Immune Cell Profiles.Cancer research communications · 2022Article
- Melatonin: Regulation of Viral Phase Separation and Epitranscriptomics in Post-Acute Sequelae of COVID-19.International journal of molecular sciences · 2022Review
- SIRT7 in the aging process.Cellular and molecular life sciences : CMLS · 2022Review
- Mitochondrial DNA and Epigenetics: Investigating Interactions with the One-Carbon Metabolism in Obesity.Oxidative medicine and cellular longevity · 2022Article
- Organ-, sex- and age-dependent patterns of endogenous L1 mRNA expression at a single locus resolution.Nucleic acids research · 2021Article
- Intercellular viral spread and intracellular transposition of Drosophila gypsy.PLoS genetics · 2021Article
- Retrotransposons as a Source of DNA Damage in Neurodegeneration.Frontiers in aging neuroscience · 2021Review
- Human L1 Transposition Dynamics Unraveled with Functional Data Analysis.Molecular biology and evolution · 2020Article
- Increasing methylation of sperm rDNA and other repetitive elements in the aging male mammalian germline.Aging cell · 2020Article
- LINE1 Derepression in Aged Wild-Type and SIRT6-Deficient Mice Drives Inflammation.Cell metabolism · 2019Article
- Engrailed homeoprotein blocks degeneration in adult dopaminergic neurons through LINE-1 repression.The EMBO journal · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Advancing age remains the largest risk factor for devastating diseases, such as heart disease, stroke, and cancer. The mechanisms by which advancing age predisposes to disease are now beginning to unfold, due in part, to genetic and environmental manipulations of longevity in lower organisms. Converging lines of evidence suggest that DNA damage may be a final common pathway linking several proposed mechanisms of aging. The present review forwards a theory for an additional aging pathway that involves modes of inherent genetic instability. Long interspersed nuclear elements (LINEs) are endogenous non-LTR retrotransposons that compose about 20% of the human genome. The LINE-1 (L1) gene products, ORF1p and ORF2p, possess mRNA binding, endonuclease, and reverse transcriptase activity that enable retrotransposition. While principally active only during embryogenesis, L1 transcripts are detected in adult somatic cells under certain conditions. The present hypothesis proposes that L1s act as an 'endogenous clock', slowly eroding genomic integrity by competing with the organism's double-strand break repair mechanism. Thus, while L1s are an accepted mechanism of genetic variation fueling evolution, it is proposed that longevity is negatively impacted by somatic L1 activity. The theory predicts testable hypotheses about the relationship between L1 activity, DNA repair, healthy aging, and longevity.
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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.