ArticleNature communications2019
Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson-Gilford Progeria Syndrome.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 121 citations in OpenAlex.
- The telomeric DNA damage response as a therapeutic target in idiopathic pulmonary fibrosis.EMBO molecular medicine · 2026Article
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Positioning TERT at the apex of aging.Nature aging · 2026Review
- Therapeutic inhibition of telomeric DNA damage response rescues hematopoietic dysfunction driven by telomere shortening and aging.Nature aging · 2026Article
- Insights into the therapeutic strategies for aging and aging-associated diseases.Signal transduction and targeted therapy · 2026Review
- Investigational New Drug-enabling studies in a human vessel-chip: Are we there yet?Bioengineering & translational medicine · 2026Review
- Article
- Molecular evolution of animal aging.The EMBO journal · 2026Review
- Review
- Telomeric DNA damage response mediates neurotoxicity of Aβ42 oligomers in Alzheimer's disease.The EMBO journal · 2025Article
- POLR3A mutations cause nucleolus abnormalities and aberrant telomerase RNA metabolism in induced pluripotent stem cells from Wiedemann-Rautenstrauch premature aging syndrome patient.Biogerontology · 2025Article
- Telomeric repeat-containing RNA increases in aged human cells.Nucleic acids research · 2025Article
- Recurrent somatic mutation and progerin expression in early vascular aging of chronic kidney disease.Nature aging · 2025Article
- ATM-dependent DNA damage response constrains cell growth and drives clonal hematopoiesis in telomere biology disorders.The Journal of clinical investigation · 2025Article
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- The complex interplay between aging and cancer.Nature aging · 2025Review
- A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches.Cancers · 2025Review
- Senescence as a therapeutic target in cancer and age-related diseases.Nature reviews. Drug discovery · 2025Review
- Premature aging and metabolic diseases: the impact of telomere attrition.Frontiers in aging · 2025Review
- Traffic light at DSB-transit regulation between gene transcription and DNA repair.FEBS letters · 2025Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomeric antisense oligonucleotides (tASOs) prevents full DDR activation and premature cellular senescence in various HGPS cell systems, including HGPS patient fibroblasts. We also show in vivo that tASO treatment significantly enhances skin homeostasis and lifespan in a transgenic HGPS mouse model. In summary, our results demonstrate an important role for telomeric DDR activation in HGPS progeroid detrimental phenotypes in vitro and in vivo.
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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.