ArticleThe EMBO journal2024
YTHDC1 delays cellular senescence and pulmonary fibrosis by activating ATR in an m6A-independent manner.
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 42 citations in OpenAlex.
- METTL3 Promotes Lipid Deposition and Pulmonary Fibrosis by Destabilizing PLIN2 in a m6A-Dependent Manner.Journal of cellular and molecular medicine · 2026Article
- Targeting alveolar type II cell dysfunction in idiopathic pulmonary fibrosis: Molecular mechanisms and emerging therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Heterologous Systems in the Functional Characterization of Proteins from Phytopathogenic Fungi: A Systematic Review.Molecular biotechnology · 2026Article
- Advances in m6A Modification in Pregnancy-Related Disorders and Female Reproductive Endocrine Diseases.Expert reviews in molecular medicine · 2026Review
- The YTHDC1-mInternational journal of oral science · 2026Article
- From Inflammation to Precision Medicine: Mechanistic Insights into Asthma, COPD, and IPF.Biomedicines · 2026Review
- Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review).International journal of molecular medicine · 2026Review
- YTH N6-methyladenosine RNA binding protein 2 mediated mMolecular biomedicine · 2026Article
- Epitranscriptomic modifications in embryonic development: insights into natural and ART-induced mechanisms and implications.Human reproduction update · 2026Review
- Total flavonoids of litchi seed attenuates cellular senescence by inhibiting the production of SASP through p65 suppression and ameliorates pulmonary fibrosis.Acta biochimica et biophysica Sinica · 2026Article
- HER3 upregulation reduces DS-8201 sensitivity in HER2-positive tumor cells by ATR/CHK1/FoxO1 signaling cascade.Acta pharmacologica Sinica · 2026Article
- N6-methyladenosine methylation in acute lung injury: Mechanisms and research progress.Journal of intensive medicine · 2026Review
- Harnessing Natural Extracellular Vesicles to Combat Age-Related Diseases: From Aging Drivers to Therapeutic Opportunities.International journal of nanomedicine · 2026Review
- Harmine Derivative H-2-104 Alleviates Echinococcus granulosus-Induced Pulmonary Fibrosis in Mice by Inhibiting Fibroblast Activation and Inducing DNA Damage.Journal of immunology research · 2026Article
- Cellular senescence in Crohn's disease: a double-edged sword in intestinal fibrosis.Frontiers in immunology · 2026Review
- The crucial role of N6-methyladenosine modification in acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Epigenetic regulatory mechanisms and translational applications in idiopathic pulmonary fibrosis.American journal of clinical and experimental immunology · 2026Review
- YBX1 regulation of alveolar type II epithelial cells in idiopathic pulmonary fibrosis: mechanistic insights and small-molecule drug screening.Journal of translational medicine · 2025Article
- Article
- Hallmarks and mechanisms of cellular senescence in aging and disease.Cell death discovery · 2025Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulation of DNA damage in the lung induces cellular senescence and promotes age-related diseases such as idiopathic pulmonary fibrosis (IPF). Hence, understanding the mechanistic regulation of DNA damage repair is important for anti-aging therapies and disease control. Here, we identified an m6A-independent role of the RNA-binding protein YTHDC1 in counteracting stress-induced pulmonary senescence and fibrosis. YTHDC1 is primarily expressed in pulmonary alveolar epithelial type 2 (AECII) cells and its AECII expression is significantly decreased in AECIIs during fibrosis. Exogenous overexpression of YTHDC1 alleviates pulmonary senescence and fibrosis independent of its m6A-binding ability, while YTHDC1 deletion enhances disease progression in mice. Mechanistically, YTHDC1 promotes the interaction between TopBP1 and MRE11, thereby activating ATR and facilitating DNA damage repair. These findings reveal a noncanonical function of YTHDC1 in delaying cellular senescence, and suggest that enhancing YTHDC1 expression in the lung could be an effective treatment strategy for pulmonary fibrosis.
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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.