ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
The relationship between complement C3 expression and the MUC5B genotype in pulmonary fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Identification of IPF specific genes expressed by lung tissue-derived fibroblasts using next generation sequencing.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- Expression of complement pathway genes is associated with progression of idiopathic pulmonary fibrosis.Respiratory research · 2026Article
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- IsERJ open research · 2025Article
- Ablation of LRP6 in alpha-smooth muscle actin-expressing cells abrogates lung inflammation and fibrosis upon bleomycin-induced lung injury.FEBS letters · 2025Article
- Complement activity and autophagy are dysregulated in the lungs of patients with nonresolvable COVID-19 requiring lung transplantation.Respiratory research · 2025Article
- Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025Review
- Ficolin-1 ameliorates pulmonary fibrosis via directly binding to TGF-β1.Journal of translational medicine · 2024Article
- Lung epithelial cell-derived C3 protects against pneumonia-induced lung injury.Science immunology · 2023Article
- siRNA-MediatedInternational journal of molecular sciences · 2023Article
- A role for the terminal C5-C9 complement pathway in idiopathic pulmonary fibrosis.Frontiers in medicine · 2023Article
- Overview on the Link Between the Complement System and Auto-Immune Articular and Pulmonary Disease.Open access rheumatology : research and reviews · 2023Review
- Our Compliments to the Authors: Decay Accelerating Factor and the Complement System in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Overexpression of Decay Accelerating Factor Mitigates Fibrotic Responses to Lung Injury.American journal of respiratory cell and molecular biology · 2022Article
- α2,6-Sialylation is Upregulated in Severe COVID-19 Implicating the Complement Cascade.medRxiv : the preprint server for health sciences · 2022Article
- Irreversibility of Pulmonary Fibrosis.Aging and disease · 2022Review
- High complement protein C1q levels in pulmonary fibrosis and non-small cell lung cancer associated with poor prognosis.BMC cancer · 2022Article
- The Epithelial-Immune Crosstalk in Pulmonary Fibrosis.Frontiers in immunology · 2021Review
- Article
- Identification of a unique temporal signature in blood and BAL associated with IPF progression.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
The common gain-of-function MUC5B promoter variant ( rs35705950 ) is the strongest risk factor for the development of idiopathic pulmonary fibrosis (IPF). While the role of complement in IPF is controversial, both MUC5B and the complement system play a role in lung host defense. The aim of this study was to evaluate the relationship between complement component 3 (C3) and MUC5B in patients with IPF and in bleomycin-induced lung injury in mice. To do this, we evaluated C3 gene expression in whole lung tissue from 300 subjects with IPF and 175 healthy controls. Expression of C3 was higher in IPF than healthy controls {1.40-fold increase [95% confidence interval (CI) 1.31-1.50]; P < 0.0001} and even greater among IPF subjects with the highest-risk IPF MUC5B promoter genotype [TT vs. GG = 1.59-fold (95% CI 1.15-2.20); P < 0.05; TT vs. GT = 1.66-fold (95% CI 1.20-2.30); P < 0.05]. Among subjects with IPF, C3 expression was significantly higher in the lung tissue without microscopic honeycombing than in the lung tissue with microscopic honeycombing [1.40-fold increase (95% CI 1.23- 1.59); P < 0.01]. In mice, while bleomycin exposure increased Muc5b protein expression, C3-deficient mice were protected from bleomycin-induced lung injury. In aggregate, our findings indicate that the MUC5B promoter variant is associated with higher C3 expression and suggest that the complement system may contribute to the pathogenesis of IPF.
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