ArticleBMC pulmonary medicine2016
Role of CD248 as a potential severity marker in idiopathic pulmonary fibrosis.
Article in BMC pulmonary medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- CD248 expression in human adipose tissue is upregulated in obesity and following glucocorticoid exposure: a mediator of insulin resistance and adipose dysfunction?Molecular medicine (Cambridge, Mass.) · 2026Article
- The CAFs-derived YAP1-periostin axis forms a fibrotic tumor microenvironment to promote metastatic lung tumor growth.Journal of translational medicine · 2026Article
- Expression of tumor endothelial marker 1 in cardiac fibroblast contributes to atrial fibrosis in atrial fibrillation.Scientific reports · 2025Article
- Genome-wide DNA methylation regulation analysis provides novel insights on post-radiation breast cancer.Scientific reports · 2025Article
- Endosialin promotes vascular maturation by inhibiting Cyr61 expression in melanoma metastasis.Frontiers in oncology · 2025Article
- Hyperbaric oxygen therapy prevents epithelial atrophy in distal tubules and TGF-β1 overexpression in diabetic rat kidneys.Journal of molecular histology · 2024Article
- Functional heterogeneity of cancer-associated fibroblasts with distinct neoadjuvant immunotherapy plus chemotherapy response in esophageal squamous cell carcinoma.Biomarker research · 2024Article
- High plasma levels of endosialin and cardiovascular events in patients undergoing coronary angiography.Heart and vessels · 2024Article
- TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts.Journal of biomedical science · 2024Article
- Comprehensive proteomic characterization of urethral stricture disease in the Chinese population.Frontiers in molecular biosciences · 2024Article
- [Expression of endosialin in human hypertrophic scars and its regulation on fibroblast phenotype].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Novel piperazine-based ionizable lipid nanoparticles allow the repeated dose of mRNA to fibrotic lungs with improved potency and safety.Bioengineering & translational medicine · 2023Article
- Inflammatory Mesenchymal Stem Cells Express Abundant Membrane-Bound and Soluble Forms of C-Type Lectin-like CD248.International journal of molecular sciences · 2023Article
- No Significant Association Between Plasma Endosialin Levels and the Presence or Severity of Coronary Artery Disease.Journal of clinical medicine research · 2022Article
- Cd248a and Cd248b in zebrafish participate in innate immune responses.Frontiers in immunology · 2022Article
- Fibrotic Idiopathic Interstitial Lung Disease: The Molecular and Cellular Key Players.International journal of molecular sciences · 2021Review
- Dissecting the Role of Mesenchymal Stem Cells in Idiopathic Pulmonary Fibrosis: Cause or Solution.Frontiers in pharmacology · 2021Review
- CD248 as a novel therapeutic target in pulmonary arterial hypertension.Clinical and translational medicine · 2020Article
- CD248 and integrin alpha-8 are candidate markers for differentiating lung fibroblast subtypes.BMC pulmonary medicine · 2020Article
- C-type lectin domain group 14 proteins in vascular biology, cancer and inflammation.The FEBS journal · 2019Review
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundCD248 or Endosialin is a transmembrane molecule expressed in stromal cells binding to extracellular matrix (ECM) components. It has been previously implicated in kidney fibrosis, rheumatoid arthritis as well as in tumour-stromal interactions. This study investigates the role of CD248 in the pathogenesis of fibrotic diseases in Idiopathic Pulmonary Fibrosis (IPF).
methodsCD248 quantitative immunohistochemistry (IHC) was performed on lung samples from 22 IPF patients and its expression was assayed in cultured pulmonary fibroblasts and epithelial cells. Effects of CD248 silencing was evaluated on fibroblast proliferation and myofibroblast differentiation.
resultsIHC revealed strong CD248 expression in mesenchymal cells of normal lung structures such as pleura and adventitia but not in epithelium. Fibrotic areas showed markedly stronger staining than unaffected lung tissue. The extent of CD248 staining showed a significant negative correlation to lung function parameters FEV1, FVC, TLC, and TLCO (r2 > 0 · 35, p < 0 · 01). CD248 protein levels were significantly greater in IPF-derived lung fibroblasts vs normal lung fibroblasts (p < 0 · 01) and CD248 silencing significantly reduced the proliferation of lung fibroblasts, but did not affected myofibroblast differentiation.
conclusionWe conclude that CD248 overexpression is possibly involved in the pathogenesis of IPF and it has potential as a disease severity marker. Given that CD248 ligands are collagen type I, IV and fibronectin, we hypothesise that CD248 signalling represents a novel matrix-fibroblast interaction that may be a potential therapeutic target in IPF.
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