ArticleJCI insight2019
Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed, 107 citations in OpenAlex.
- Skeletal Muscle Dysfunction and Exercise Intolerance in COPD and Idiopathic Pulmonary Fibrosis: Extracellular Vesicles as Candidate Mediators of a Lung-Muscle Axis.Muscles (Basel, Switzerland) · 2026Review
- Co-optation of the regenerative role of type 2 alveolar cells in distal lung repair in mice by terminal airway epithelial cells in humans.bioRxiv : the preprint server for biology · 2026Article
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- Macropinocytosis inhibition attenuates profibrotic responses in lung fibroblasts and pulmonary fibrosis models.The Journal of clinical investigation · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Syndecan-1 Promotes Alveolar Type 2 Epithelial Cell Senescence during Lung Fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Extracellular vesicles from alveolar macrophages promotes pulmonary fibrosis through suppression of lung alveolar regeneration.Journal of nanobiotechnology · 2026Article
- Integrated miR-omics and proteomics reveal the regulatory role of miR in protein networks associated with COVID-19 disease progression.Frontiers in immunology · 2026Article
- Myofibroblast-Derived Extracellular Vesicles Drive Profibrotic Cascade Amplification in Pulmonary Fibrosis via the Nestin-Rab7 Axis.Journal of extracellular vesicles · 2026Article
- Article
- Extracellular Vesicles: Multimodal Tools for Diagnosis, Prognosis, and Therapy in Respiratory Diseases.Expert reviews in molecular medicine · 2025Review
- A mesothelial differentiation gateway drives fibrosis.Nature communications · 2025Article
- Evidence that metformin promotes fibrosis resolutionActa pharmaceutica Sinica. B · 2025Article
- Enhanced THBS2 promotes collagen synthesis and inflammatory secretome of fibroblasts in idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Tregs.JCI insight · 2025Article
- Serum syndecan-1 is related to severity and prognosis of COVID-19 patients: a perspective cohort study.BMC pulmonary medicine · 2025Article
- Vascular protection by young circulating extracellular vesicles ameliorates aging-related pulmonary fibrosis.American journal of physiology. Cell physiology · 2025Article
- Exosomes are specialized vehicles to induce fibronectin assembly.bioRxiv : the preprint server for biology · 2025Article
- Article
- Burn-Related Glycocalyx Derangement and the Emerging Role of MMP8 in Syndecan Shedding.Biology · 2025Article
8 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
20 authors at 6 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic and fatal lung disease. A maladaptive epithelium due to chronic injury is a prominent feature and contributor to pathogenic cellular communication in IPF. Recent data highlight the concept of a "reprogrammed" lung epithelium as critical in the development of lung fibrosis. Extracellular vesicles (EVs) are potent mediator of cellular crosstalk, and recent evidence supports their role in lung pathologies such as IPF. Here, we demonstrate that syndecan-1 is overexpressed by the epithelium in the lungs of IPF patients and in murine models after bleomycin injury. Moreover, we find that syndecan-1 is a pro-fibrotic signal that alters alveolar type II (ATII) cell phenotypes by augmenting TGFβ and Wnt signaling among other pro-fibrotic pathways. Importantly, we demonstrate that syndecan-1 controls the packaging of several anti-fibrotic microRNAs into EVs that have broad effects over several fibrogenic signaling networks as a mechanism of regulating epithelial plasticity and pulmonary fibrosis. Collectively, our work reveals new insight into how EVs orchestrate cellular signals that promote lung fibrosis and demonstrate the importance of syndecan-1 in coordinating these programs.
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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.