ArticleRegenerative biomaterials2025
Fibrotic lung ECM upregulates SDC4/integrin-αvβ1 interaction and the interfering peptide SDC4
Article in Regenerative biomaterials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
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
1 citing paper in PubMed.
- Unlocking the potential of mRNA nanomedicines for comprehensive fibrosis therapy.Molecular therapy. Nucleic acids · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Fibroblast activation promotes remodeling of the extracellular matrix (ECM), and the fibrotic remodeling ECM further stimulating fibroblast activation and advancing pulmonary fibrosis (PF). syndecan-4 (SDC4) is the key mediator of ECM-cell signaling, but its action in PF remains unclear. Using decellularized lung ECM (dECM), this study found that fibrotic ECM enhanced fibroblast activation via SDC4-regulated integrin-αvβ1 expression and activation, and FAK/AKT phosphorylation. Meanwhile, SDC4 knockdown inhibited fibrotic ECM-induced TGF-β1 synthesis and PKCα activation. A Duolink-proximity ligation assay confirmed extracellular interactions between SDC4 and integrin-αvβ1, and the SDC4 blocking antibody Anti-SDC4
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