ArticleiScience2025
Syndecan-1-mediated loading of VEGF-A into small extracellular vesicles facilitates peritubular capillary repair during AKI-to-CKD transition.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Elevated Serum Soluble Syndecan-1 Is Associated with Lupus Nephritis Flares: A Cross-Sectional Study.International journal of molecular sciences · 2026Article
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Authors and funding
9 authors.
Funding
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Abstract
Acute kidney injury (AKI) is a severe clinical event with a high risk of transitioning to chronic kidney disease (CKD). Persistent hypoxia resulting from peritubular capillaries (PTCs) loss is a key factor driving this chronic transition. However, the mechanisms governing PTCs injury and repair, particularly under different AKI severity, remain unclear. This study demonstrates that small extracellular vesicle (sEV) carried VEGF-A as an essential regulator of PTCs repair and decreased as the severity of tubular injury increased. We found that VEGF-A was sorted into sEV via syndecan-1 (SDC-1), attaching to the heparan sulfate chain in moderate AKI. SDC-1 knockdown in renal tubules significantly reduced VEGF-A packaging into EVs and aggravated PTCs rarefaction and renal fibrosis. Overexpression of SDC-1 promoted the production of VEGF-A
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Registered trials
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