ArticleNature aging2024
Reactivation of senescence-associated endogenous retroviruses by ATF3 drives interferon signaling in aging.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- The ancient viral whispers of ageing: awakening the dark genome.Life medicine · 2026Article
- Review
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Investigating the human anellome across the lifespan reveals sex-specific biphasic trajectories.npj aging · 2026Article
- Intracellular Calcium Overload Promotes NFATc1-ATF3 Activation and Induces the Senescence-Associated Phenotype in Irradiated Osteocytes.Life (Basel, Switzerland) · 2026Article
- Immunological consequences of senescence in physiology and pathology.Journal of translational medicine · 2026Review
- Ectopic co-expression of canonical and LINE1 and THE1A-exonizing IL23R transcripts in sarcoid myopathy.Journal of human genetics · 2026Article
- AUF1 modulates cellular senescence in auditory hair cells by regulating the transcription and alternative splicing of immune response genes.Molecular biology reports · 2026Article
- Betrixaban activates cGAS and ERVs to promote dual nucleic-sensing antiviral immunity.EMBO molecular medicine · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 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
- RETRACTED: Endogenous Retroviruses as Regulators of Innate Immune Signaling and InflammationViruses · 2026Review
- ICE: robust detection of cellular senescence from weak single-cell signatures using imputation-based marker refinement.Genome biology · 2026Article
- CDK9 Inhibition with enitociclib reveals influence on HERV and LINE RNA abundances in whole blood, T-, and B-Cell lines.BMC medical genomics · 2026Article
- The inflammatory clock: how cGAS-STING ticks in the aging ovary.Frontiers in cell and developmental biology · 2026Review
- LINE-1 retrotransposition in a mouse TDP-43 model of neurodegeneration marks motor cortex neurons for cell-intrinsic and cell non-autonomous programmed cell death.PLoS genetics · 2025Article
- DNA fragmentation factor B suppresses interferon to enable cancer persister cell regrowth.Nature cell biology · 2025Article
- Biomarkers of ageing of humans and non-human primates.Nature reviews. Molecular cell biology · 2025Review
- Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease.Nature reviews. Molecular cell biology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Reactivation of endogenous retroviruses (ERVs) has been proposed to be involved in aging. However, the mechanism of reactivation and contribution to aging and age-associated diseases is largely unexplored. In this study, we identified a subclass of ERVs reactivated in senescent cells (termed senescence-associated ERVs (SA-ERVs)). These SA-ERVs can be bidirectional transcriptionally activated by activating transcription factor 3 (ATF3) to generate double-stranded RNAs (dsRNAs), which activate the RIG-I/MDA5-MAVS signaling pathway and trigger a type I interferon (IFN-I) response in senescent fibroblasts. Consistently, we found a concerted increased expression of ATF3 and SA-ERVs and enhanced IFN-I response in several tissues of healthy aged individuals and patients with Hutchinson-Gilford progeria syndrome. Moreover, we observed an accumulation of dsRNAs derived from SA-ERVs and higher levels of IFNβ in blood of aged individuals. Together, these results reveal a previously unknown mechanism for reactivation of SA-ERVs by ATF3 and illustrate SA-ERVs as an important component and hallmark of aging.
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