ReviewCommunications biology2024
Replication stress as a driver of cellular senescence and aging.
Review in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The relationship between physical activity and telomere length in women: A systematic review.Mechanisms of ageing and development · 2025Pooled it
- Repair and misrepair of telomeric DNA in dynamic interactions with PML nuclear bodies and lamin B1 in doxorubicin-treated cancer cells.Nucleus (Austin, Tex.) · 2026Article
- Senescent Cell Heterogeneity: Tissue-Dependent Signatures and Age Dynamics Revealed by Human scRNA-Seq Data.International journal of molecular sciences · 2026Article
- Plant-specific and conserved mechanisms of the polymerase-associated factor 1 complex in replication stress responses.Nature plants · 2026Article
- Proteomic Characterization of Replication Stress and Impaired Antioxidant Defense in Tacrolimus-Induced Chronic Nephrotoxicity.International journal of molecular sciences · 2026Article
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development.iScience · 2026Article
- Review
- Regenerative Approaches to Enhance the Skin Microenvironment and Boost Aesthetic Efficacy: A Narrative Review.International journal of molecular sciences · 2026Review
- Targeting RNase H2: A dual-mechanism strategy to elevate replication stress, DNA damage, and antitumor immunity in TNBC.Cell reports. Medicine · 2026Article
- Loss of endothelial miR-126 drives age-related decline in hematopoiesis.Haematologica · 2026Article
- Targeting the pMHC-TCR Interaction: Molecular Strategies and Therapeutic Potential in Autoimmunity.International journal of molecular sciences · 2026Review
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Subtle-seq reveals frequent ageing-associated chromosome fragmentation on nucleosome core DNA.Nucleic acids research · 2026Article
- Article
- Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence.Nature aging · 2026Article
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
- Article
- The Role of Cellular Senescence in Oral Health and Disease.International journal of molecular sciences · 2026Review
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
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.
Funding
Abstract
Replication stress refers to slowing or stalling of replication fork progression during DNA synthesis that disrupts faithful copying of the genome. While long considered a nexus for DNA damage, the role of replication stress in aging is under-appreciated. The consequential role of replication stress in promotion of organismal aging phenotypes is evidenced by an extensive list of hereditary accelerated aging disorders marked by molecular defects in factors that promote replication fork progression and operate uniquely in the replication stress response. Additionally, recent studies have revealed cellular pathways and phenotypes elicited by replication stress that align with designated hallmarks of aging. Here we review recent advances demonstrating the role of replication stress as an ultimate driver of cellular senescence and aging. We discuss clinical implications of the intriguing links between cellular senescence and aging including application of senotherapeutic approaches in the context of replication stress.
Indexed as
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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.