ArticleNature communications2020
Telomere dysfunction activates YAP1 to drive tissue inflammation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Single-cell transcriptomics highlights immunological dysregulations of monocytes in the pathobiology of COPD.Respiratory research · 2022Pooled it
- STING deficiency does not rescue short telomere-mediated aging phenotypes and longevity in TERC- or TERT-telomerase deficient mice.Cell reports · 2026Article
- Positioning TERT at the apex of aging.Nature aging · 2026Review
- The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.Biological reviews of the Cambridge Philosophical Society · 2026Review
- The Regulation and Function of Hippo/YAP Pathway in Cancer.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Article
- Review
- MiR-509-3p Targets YAP1 to Regulate Inflammatory Cytokines Against Hyperglycemia-Induced Renal Tubular Cell Damage in Diabetic Kidney Disease.Combinatorial chemistry & high throughput screening · 2026Article
- The hippo pathway: a molecular bridge between environmental cues and pace of life.BMC ecology and evolution · 2025Review
- Delaying liver aging: Analysis of structural and functional alterations.World journal of gastroenterology · 2025Article
- The relationship between telomere length and aging-related diseases.Clinical and experimental medicine · 2025Review
- Review
- A telomere-associated molecular landscape reveals immunological, microbial, and therapeutic heterogeneity in colorectal cancer.Frontiers in molecular biosciences · 2025Article
- The Anti-Elixir Triad: Non-Synced Circadian Rhythm, Gut Dysbiosis, and Telomeric Damage.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025Review
- A living organoid biobank of patients with Crohn's disease reveals molecular subtypes for personalized therapeutics.Cell reports. Medicine · 2024Article
- A highly sensitive reporter system to monitor endogenous YAP1/TAZ activity and its application in various human cells.Cancer science · 2024Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Article
- Tumor Promoters and Opportunities for Molecular Cancer Prevention.Cancer discovery · 2024Review
- Monoclonal Antibodies Against Mature Interleukin-18 Ameliorate Colitis and Repair Goblet Cell Function.Digestive diseases and sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
36 authors at 7 institutions in 3 countries.
Funding
Abstract
Germline telomere maintenance defects are associated with an increased incidence of inflammatory diseases in humans, yet whether and how telomere dysfunction causes inflammation are not known. Here, we show that telomere dysfunction drives pATM/c-ABL-mediated activation of the YAP1 transcription factor, up-regulating the major pro-inflammatory factor, pro-IL-18. The colonic microbiome stimulates cytosolic receptors activating caspase-1 which cleaves pro-IL-18 into mature IL-18, leading to recruitment of interferon (IFN)-γ-secreting T cells and intestinal inflammation. Correspondingly, patients with germline telomere maintenance defects exhibit DNA damage (γH2AX) signaling together with elevated YAP1 and IL-18 expression. In mice with telomere dysfunction, telomerase reactivation in the intestinal epithelium or pharmacological inhibition of ATM, YAP1, or caspase-1 as well as antibiotic treatment, dramatically reduces IL-18 and intestinal inflammation. Thus, telomere dysfunction-induced activation of the ATM-YAP1-pro-IL-18 pathway in epithelium is a key instigator of tissue inflammation.
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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.