ArticleCell death and differentiation2019
Genomic stability, anti-inflammatory phenotype, and up-regulation of the RNAseH2 in cells from centenarians.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- The long-lived immune system of centenarians.Nature reviews. Immunology · 2026Review
- The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Bat-Inspired Longevity: Immune Damage Management and Nutritional Modulation for Healthy Aging.International journal of molecular sciences · 2026Review
- Mechanistic redundancy and hierarchy of aging mechanisms: implications for strategies to extend healthspan and biomarker integration.Frontiers in aging · 2026Review
- POLR3A mutations cause nucleolus abnormalities and aberrant telomerase RNA metabolism in induced pluripotent stem cells from Wiedemann-Rautenstrauch premature aging syndrome patient.Biogerontology · 2025Article
- Age-related and postmenopausal breast cancer progression and treatment management: The significance of pro-inflammatory cytokines and CXC chemokines.Genes & diseases · 2025Review
- Toward precision interventions and metrics of inflammaging.Nature aging · 2025Review
- MicroRNA‑96 promotes the proliferation and migration of breast cancer cells by inhibiting Smad7 expression.Oncology letters · 2025Article
- Cardiac vagal control and inflammation are upregulated in exceptional human longevity.Internal and emergency medicine · 2025Article
- Ribosomal DNA and Neurological Disorders.Current molecular medicine · 2025Review
- Transcriptomic analysis revealed that oar-miR-370-3p was involved in the regulation of wool fineness in Ordos fine-wool sheep.Frontiers in veterinary science · 2025Article
- Cross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.Bone research · 2024Review
- Replicative senescence and high glucose induce the accrual of self-derived cytosolic nucleic acids in human endothelial cells.Cell death discovery · 2024Article
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- Longevity-Associated Transcription Factor ATF7 Promotes Healthspan by Suppressing Cellular Senescence and Systematic Inflammation.Aging and disease · 2023Article
- Dauer larva-derived extracellular vesicles extend the life of Caenorhabditis elegans.Biogerontology · 2023Article
- Pro-inflammatory RNA:DNA Hybrids Are p53 Independently Boosted by Hyperbaric Oxygen: a Subcellular Distribution Analysis by Automated Quantitative Imaging.Molecular imaging and biology · 2023Article
- Extracellular Vesicles as "Very Important Particles" (VIPs) in Aging.International journal of molecular sciences · 2023Review
- Development of an RNase H2 Activity Assay for Clinical Screening.Journal of clinical medicine · 2023Article
- Longevity, Centenarians and Modified Cellular Proteodynamics.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current literature agrees on the notion that efficient DNA repair favors longevity across evolution. The DNA damage response machinery activates inflammation and type I interferon signaling. Both pathways play an acknowledged role in the pathogenesis of a variety of age-related diseases and are expected to be detrimental for human longevity. Here, we report on the anti-inflammatory molecular make-up of centenarian's fibroblasts (low levels of IL-6, type 1 interferon beta, and pro-inflammatory microRNAs), which is coupled with low level of DNA damage (measured by comet assay and histone-2AX activation) and preserved telomere length. In the same cells, high levels of the RNAseH2C enzyme subunit and low amounts of RNAseH2 substrates, i.e. cytoplasmic RNA:DNA hybrids are present. Moreover, RNAseH2C locus is hypo-methylated and RNAseH2C knock-down up-regulates IL-6 and type 1 interferon beta in centenarian's fibroblasts. Interestingly, RNAseH2C locus is hyper-methylated in vitro senescent cells and in tissues from atherosclerotic plaques and breast tumors. Finally, extracellular vesicles from centenarian's cells up-regulate RNAseH2C expression and dampen the pro-inflammatory phenotype of fibroblasts, myeloid, and cancer cells. These data suggest that centenarians are endowed with restrained DNA damage-induced inflammatory response, that may facilitate their escape from the deleterious effects of age-related chronic inflammation.
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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.