#LINE1Retrotransposons
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LINE-1 Retrotransposon Derepression in Aging Tissues: Publication Trend Analysis (2015–2024)

#LINE1Retrotransposons #TransposableElements #EpigeneticAging #HeterchromatinErosion #cGASSTING #CellularSenescence #RepetitiveElementBiology #GenomicInstability
LINE-1 Retrotransposon Derepression in Aging Tissues: Publication Trend Analysis (2015–2024) The PubMed bibliometric data for LINE-1 retrotransposon derepression in aging tissues reveals a field that has undergone a discernible but restrained growth trajectory over the past decade, with an apparent plateau emerging after approximately 2021. Beginning at a low baseline of 3 publications in 2015, output remained modest and inconsistent through 2018, consistent with a pre-paradigmatic phase in which mechanistic frameworks—particularly those connecting heterochromatin erosion, loss of DNMT1/3a-mediated CpG methylation at L1 5' UTR promoters, and downstream innate immune activation via cGAS-STING—were still being consolidated from disparate lines of evidence. The notable inflection between 2018 and 2021, peaking at 8 publications, temporally correlates with several convergent developments: the demonstration that age-associated H3K9me3 depletion at L1 loci facilitates ORF1p and ORF2p expression in somatic tissues, the characterization of L1-derived reverse transcription intermediates as cGAS ligands, and the mechanistic linking of L1 reactivation to the sterile inflammatory phenotype characteristic of cellular senescence and the senescence-associated secretory phenotype (SASP). The stabilization at 6–8 publications annually from 2021 onward is analytically informative and warrants careful interpretation rather than dismissal. It does not straightforwardly indicate decline or saturation of scientific interest. Rather, it may reflect a field entering a phase of methodological and conceptual consolidation, wherein the primary mechanistic axes—epigenetic derepression via loss of repressive chromatin marks, retrotransposition-competent versus retrotransposition-incompetent L1 element activity, nucleic acid sensing pathway engagement, and tissue-specific permissiveness to L1 expression during aging.
June 2, 2026 at 5:03 PM