ArticleCell communication and signaling : CCS2024
DEC1 is involved in circadian rhythm disruption-exacerbated pulmonary fibrosis.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 2 citations in OpenAlex.
- Application of Circadian Rhythm-Based Pulmonary Rehabilitation in Patients with Severe Pneumonia-A Feasibility Study With Convenience Sampling.Archives of rehabilitation research and clinical translation · 2026Article
- Circadian disruption and cellular senescence: emerging perspectives in periodontitis.Odontology · 2026Review
- Circadian Rhythms in Acute Respiratory Distress Syndrome: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Targeting Circadian Rhythm Disruption in Glaucoma: PTGDS Mediates Trabecular Meshwork Fibrosis and Is Therapeutically Targeted by Aprepitant.Translational vision science & technology · 2026Article
- Circadian clock regulation in lung health and disease: molecular mechanisms and therapeutic opportunities.EXCLI journal · 2026Review
- mJournal of translational medicine · 2025Article
- Review
- [Mechanism of melatonin regulating the expression level of rhythm genes to alleviate interstitial pulmonary fibrosis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe alveolar epithelial type II cell (AT2) and its senescence play a pivotal role in alveolar damage and pulmonary fibrosis. Cell circadian rhythm is strongly associated with cell senescence. Differentiated embryonic chondrocyte expressed gene 1 (DEC1) is a very important circadian clock gene. However, the role of DEC1 in AT2 senescence and pulmonary fibrosis was still unclear.
resultsIn this study, a circadian disruption model of light intervention was used. It was found that circadian disruption exacerbated pulmonary fibrosis in mice. To understand the underlying mechanism, DEC1 levels were investigated. Results showed that DEC1 levels increased in lung tissues of IPF patients and in bleomycin-induced mouse fibrotic lungs. In vitro study revealed that bleomycin and TGF-β1 increased the expressions of DEC1, collagen-I, and fibronectin in AT2 cells. Inhibition of DEC1 mitigated bleomycin-induced fibrotic changes in vitro and in vivo. After that, cell senescence was observed in bleomycin-treated AT2 cells and mouse models, but these were prevented by DEC1 inhibition. At last, p21 was confirmed having circadian rhythm followed DEC1 in normal conditions. But bleomycin disrupted the circadian rhythm and increased DEC1 which promoted p21 expression, increased p21 mediated AT2 senescence and pulmonary fibrosis.
conclusionsTaken together, circadian clock protein DEC1 mediated pulmonary fibrosis via p21 and cell senescence in alveolar epithelial type II cells.
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