ArticleThe Journal of clinical investigation2010
Inhibition of pulmonary fibrosis in mice by CXCL10 requires glycosaminoglycan binding and syndecan-4.
Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
104 citing papers in PubMed, 165 citations in OpenAlex.
- Smoking decreases the response of human lung macrophages to double-stranded RNA by reducing TLR3 expression.Respiratory research · 2013Trial
- Dual roles of syndecan-4 in regulating chicken fibrosisFrontiers in physiology · 2026Article
- β-III tubulin identifies anti-fibrotic state of pericytes in pulmonary fibrosis.Research square · 2025Article
- β-III tubulin identifies anti-fibrotic state of pericytes in pulmonary fibrosis.bioRxiv : the preprint server for biology · 2025Article
- Targeting E3 ubiquitin ligases: a new frontier in idiopathic pulmonary fibrosis treatment.Frontiers in immunology · 2025Review
- Fibrotic lung ECM upregulates SDC4/integrin-αvβ1 interaction and the interfering peptide SDC4Regenerative biomaterials · 2025Article
- Review
- Oleic Acid Inhibits SDC4 and Promotes Ferroptosis in Lung Cancer Through GPX4/ACSL4.The clinical respiratory journal · 2024Article
- Article
- CXCR3-independent role of CXCL10 in alveolar epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- EphB2 Receptor Promotes Dermal Fibrosis in Systemic Sclerosis.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity.Cell communication and signaling : CCS · 2024Article
- Identifying health risk determinants and molecular targets in patients with idiopathic pulmonary fibrosis via combined differential and weighted gene co-expression analysis.Frontiers in genetics · 2024Article
- SRC and TKS5 mediated podosome formation in fibroblasts promotes extracellular matrix invasion and pulmonary fibrosis.Nature communications · 2023Article
- Identification of memory B-cell-associated miRNA signature to establish a prognostic model in gastric adenocarcinoma.Journal of translational medicine · 2023Article
- Distribution and chemotactic mechanism of CD4Immunity, inflammation and disease · 2023Article
- A review of the pleiotropic actions of the IFN-inducible CXC chemokine receptor 3 ligands in the synovial microenvironment.Cellular and molecular life sciences : CMLS · 2023Review
- Old age promotes retinal fibrosis in choroidal neovascularization through circulating fibrocytes and profibrotic macrophages.Journal of neuroinflammation · 2023Article
- Endothelial Damage and the Microcirculation in Critical Illness.Biomedicines · 2022Review
- Chemokine CCL9 Is Upregulated Early in Chronic Kidney Disease and Counteracts Kidney Inflammation and Fibrosis.Biomedicines · 2022Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Pulmonary fibrosis is a progressive, dysregulated response to injury culminating in compromised lung function due to excess extracellular matrix production. The heparan sulfate proteoglycan syndecan-4 is important in mediating fibroblast-matrix interactions, but its role in pulmonary fibrosis has not been explored. To investigate this issue, we used intratracheal instillation of bleomycin as a model of acute lung injury and fibrosis. We found that bleomycin treatment increased syndecan-4 expression. Moreover, we observed a marked decrease in neutrophil recruitment and an increase in both myofibroblast recruitment and interstitial fibrosis in bleomycin-treated syndecan-4-null (Sdc4-/-) mice. Subsequently, we identified a direct interaction between CXCL10, an antifibrotic chemokine, and syndecan-4 that inhibited primary lung fibroblast migration during fibrosis; mutation of the heparin-binding domain, but not the CXCR3 domain, of CXCL10 diminished this effect. Similarly, migration of fibroblasts from patients with pulmonary fibrosis was inhibited in the presence of CXCL10 protein defective in CXCR3 binding. Furthermore, administration of recombinant CXCL10 protein inhibited fibrosis in WT mice, but not in Sdc4-/- mice. Collectively, these data suggest that the direct interaction of syndecan-4 and CXCL10 in the lung interstitial compartment serves to inhibit fibroblast recruitment and subsequent fibrosis. Thus, administration of CXCL10 protein defective in CXCR3 binding may represent a novel therapy 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.