ArticlePloS one2022
The role of eCIRP in bleomycin-induced pulmonary fibrosis in mice.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Increased Serum Cold-Inducible RNA-Binding Protein Levels in Psoriasis.Annals of dermatology · 2026Article
- Radiation-induced eCIRP Causes Alzheimer's Disease-like Neuronal Tau Phosphorylation.Molecular neurobiology · 2026Article
- Cold inducible RNA binding protein promotes fibroblast activation and its inhibition represents a potential therapeutic target in pulmonary fibrosis.Scientific reports · 2026Article
- The Role of Cold-Inducible RNA-Binding Protein (CIRP) in Neurological Disorders.Brain sciences · 2026Review
- Retinal ALKBH5 inhibition induces myopia protection through selective regulation of ERK1/2 signaling.Journal of translational medicine · 2025Article
- Inhibition of eCIRP attenuates PANoptosis and renal fibrosis.American journal of physiology. Renal physiology · 2025Article
- Extracellular Cold-Inducible RNA-Binding Protein: Progress from Discovery to Present.International journal of molecular sciences · 2025Review
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- C23 ameliorates carbon tetrachloride-induced liver fibrosis in mice.World journal of hepatology · 2024Article
- Serum concentration of extracellular cold-inducible RNA-binding protein is associated with respiratory failure in COVID-19.Frontiers in immunology · 2022Observational
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
OBJECTIVE AND
designWe examined the role of eCIRP in the pathogenesis of bleomycin-induced pulmonary fibrosis (PF). MATERIAL AND
methodsPublicly available gene expression omnibus datasets were analyzed for the expression of CIRP in lung samples from patients with PF. Wild type (WT) or CIRP-/- mice received daily injections of 10 μg/g bleomycin for 10 days. A subset of bleomycin-injected WT mice was treated with the eCIRP antagonist C23 (8 μg/g/day) from day 10 to day 19. At three weeks, transthoracic echocardiography was performed to measure the degree of pulmonary hypertension, and lung tissues were collected and analyzed for markers of fibrosis.
resultsAnalysis of the mRNA data of human lung samples showed a significant positive correlation between CIRP and α-smooth muscle actin (α-SMA), an important marker of fibrosis. Moreover, the expression of CIRP was higher in patients with acute exacerbation of PF than in patients with stable PF. CIRP-/- mice showed attenuated induction of α-SMA and collagens (Col1a1, Col3a1), reduced hydroxyproline content, decreased histological fibrosis scores, and improved pulmonary hypertension as compared to WT mice. WT mice treated with C23 also had significant attenuation of the above endpoint measure.
conclusionsOur study demonstrates that eCIRP plays a key role in promoting the development of PF, and blocking eCIRP with C23 can significantly attenuate this process.
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