ArticleInternational journal of molecular sciences2019
Syndecan-4 Inhibits the Development of Pulmonary Fibrosis by Attenuating TGF-β Signaling.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Decoding cellular communication networks and signaling pathways in bone, skeletal muscle, and bone-muscle crosstalk through spatial transcriptomics in a young male mouse.Bone research · 2026Article
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- Effect of altitudes on serum parameters, metabolome, and gut microbiota in yaks on the Qinghai-Tibet Plateau.Microbiology spectrum · 2026Article
- Dual roles of syndecan-4 in regulating chicken fibrosisFrontiers in physiology · 2026Article
- Midkine Deficiency Attenuates Lipopolysaccharide-Induced Pulmonary Inflammation.International journal of molecular sciences · 2025Article
- Shed Syndecan-4 and Its Possible Roles in Osteoarthritis.Biomedicines · 2025Review
- Syndecan-1 Plays a Role in the Pathogenesis of Sjögren's Disease by Inducing B-Cell Chemotaxis through CXCL13-Heparan Sulfate Interaction.International journal of molecular sciences · 2024Article
- Targeted Antisense Oligonucleotide-Mediated Skipping of MurineInternational journal of molecular sciences · 2024Article
- Roles of extracellular matrix in lung diseases.Fukushima journal of medical science · 2024Review
- APP-CD74 axis mediates endothelial cell-macrophage communication to promote kidney injury and fibrosis.Frontiers in pharmacology · 2024Article
- Novel cardiac extracellular matrix biomarkers in STEMI: Associations with ischemic injury and long-term mortality.PloS one · 2024Article
- Systemically administered wound-homing peptide accelerates wound healing by modulating syndecan-4 function.Nature communications · 2023Article
- Serum Osteopontin, KL-6, and Syndecan-4 as Potential Biomarkers in the Diagnosis of Coal Workers' Pneumoconiosis: A Case-Control Study.Pharmacogenomics and personalized medicine · 2023Article
- Endothelial Damage and the Microcirculation in Critical Illness.Biomedicines · 2022Review
- Keloid Biomarkers and Their Correlation With Immune Infiltration.Frontiers in genetics · 2022Article
- Research Progress in the Molecular Mechanisms, Therapeutic Targets, and Drug Development of Idiopathic Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- How Do We Know What We Are Missing? Loss of Signaling through CD148 Drives Fibroblast Activation in Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021Article
- Syndecan receptors: pericellular regulators in development and inflammatory disease.Open biology · 2021Review
- Potential therapeutic manipulations of the CXCR3 chemokine axis for the treatment of inflammatory fibrosing diseases.F1000Research · 2020Article
- Syndecans in Inflammation at a Glance.Frontiers in immunology · 2020Review
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Syndecan-4 is a transmembrane heparan sulfate proteoglycan expressed in a variety of cells, and its heparan sulfate glycosaminoglycan side chains bind to several proteins exhibiting various biological roles. The authors have previously demonstrated syndecan-4's critical roles in pulmonary inflammation. In the current study, however, its role in pulmonary fibrosis was evaluated. Wild-type and syndecan-4-deficient mice were injected with bleomycin, and several parameters of inflammation and fibrosis were analyzed. The mRNA expression of collagen and α-smooth muscle action (α-SMA) in lung tissues, as well as the histopathological lung fibrosis score and collagen content in lung tissues, were significantly higher in the syndecan-4-deficient mice. However, the total cell count and cell differentiation in bronchoalveolar lavage fluid were equivalent between the wild-type and syndecan-4-deficient mice. Although there was no difference in the TGF-β expression in lung tissues between the wild-type and syndecan-4-deficient mice, significantly more activation of Smad3 in lung tissues was observed in the syndecan-4-deficient mice compared to the wild-type mice. Furthermore, in the in vitro experiments using lung fibroblasts, the co-incubation of syndecan-4 significantly inhibited TGF-β-induced Smad3 activation, collagen and α-SMA upregulation. Moreover, syndecan-4 knock-down by siRNA increased TGF-β-induced Smad3 activation and upregulated collagen and α-SMA expression. These findings showed that syndecan-4 inhibits the development of pulmonary fibrosis, at least in part, through attenuating TGF-β signaling.
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