ArticleAging2019
Epithelial cell senescence induces pulmonary fibrosis through Nanog-mediated fibroblast activation.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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Who cites it
42 citing papers in PubMed, 59 citations in OpenAlex.
- Cellular Senescence: Emerging Therapeutic Target for Idiopathic Pulmonary Fibrosis Pathogenic Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2026Review
- The senescence-inhibitory p53 isoform Δ133p53α: enhancing cancer immunotherapy and exploring novel therapeutic approaches for senescence-associated diseases.GeroScience · 2026Review
- Immortalization of Human Adult Alveolar Epithelial Cells to Study Environmental Exposures of the Distal Lung.Current protocols · 2026Article
- The Microbial Metabolite IDA Sensitizes Tumor Cells to ARF1 Inhibition by Inducing SVIL-dependent Senescence.International journal of biological sciences · 2026Article
- Emerging Mechanistic Links Between Fucosylation and Senescence in Lung Diseases.Journal of respiratory biology and translational medicine · 2026Article
- Wnt signaling pathway in lung aging and aging-related chronic lung diseases.Biogerontology · 2025Review
- Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025Review
- Predictive and personalized approaches for idiopathic pulmonary fibrosis: a Wnt-related gene set scoring framework integrating single-cell sequencing, spatial transcriptomics, and machine learning for diagnosis and prognosis.Functional & integrative genomics · 2025Article
- CT-sensitized nanoprobe for effective early diagnosis and treatment of pulmonary fibrosis.Journal of nanobiotechnology · 2025Article
- SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis.Frontiers in cell and developmental biology · 2025Review
- ModulatingAging · 2024Article
- Addition of Polyphenols to Drugs: The Potential of Controlling "Inflammaging" and Fibrosis in Human Senescent Lung Fibroblasts In Vitro.International journal of molecular sciences · 2024Article
- Exosomes from senescent epithelial cells activate pulmonary fibroblasts via the miR-217-5p/Sirt1 axis in paraquat-induced pulmonary fibrosis.Journal of translational medicine · 2024Article
- Vitamin C, doxycycline, and azithromycin (VDA) targeted changes in cellular senescence-related genes in human adipose-derived mesenchymal stem cells.Iranian journal of basic medical sciences · 2024Article
- Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Adenine nucleotide carrier protein dysfunction in human disease.IUBMB life · 2023Review
- Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.American journal of physiology. Cell physiology · 2023Review
- Article
- Calcium oxalate crystal-induced secretome derived from proximal tubular cells, not that from distal tubular cells, induces renal fibroblast activation.European journal of medical research · 2023Article
- Impaired autophagy-accelerated senescence of alveolar type II epithelial cells drives pulmonary fibrosis induced by single-walled carbon nanotubes.Journal of nanobiotechnology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease tightly correlated with aging. The pathological features of IPF include epithelial cell senescence and abundant foci of highly activated pulmonary fibroblasts. However, the underlying mechanism between epithelial cell senescence and pulmonary fibroblast activation remain to be elucidated. In our study, we demonstrated that Nanog, as a pluripotency gene, played an essential role in the activation of pulmonary fibroblasts. In the progression of IPF, senescent epithelial cells could contribute to the activation of pulmonary fibroblasts via increasing the expression of senescence-associated secretory phenotype (SASP). In addition, we found activated pulmonary fibroblasts exhibited aberrant activation of Wnt/β-catenin signalling and elevated expression of Nanog. Further study revealed that the activation of Wnt/β-catenin signalling was responsible for senescent epithelial cell-induced Nanog phenotype in pulmonary fibroblasts. β-catenin was observed to bind to the promoter of Nanog during the activation of pulmonary fibroblasts. Targeted inhibition of epithelial cell senescence or Nanog could effectively suppress the activation of pulmonary fibroblasts and impair the development of pulmonary fibrosis, indicating a potential for the exploration of novel anti-fibrotic strategies.
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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.