Hypoxic ADSC Exosomes Alleviate Primary Sjögren's Syndrome-Induced Skin Injury via GLRX2 Delivery and Ferroptosis Suppression.
Wang X., Wu F., Yang X., Yang H., Xu G., Chen R.
Animal Study, published in Immunol Invest (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Immunol Invest (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40492693
- DOI
- 10.1080/08820139.2025.2516671
- Citations
- 1
Abstract (original English)
Background The aim of the present study was to assess the therapeutic effects of ADSC-Exos for SS-induced skin injury. Methods A mouse model of SS was constructed and Exos from ADSCs (Exos) and hypoxia-pretreated ADSCs (HExos) were isolated. The therapeutic effects of Exos were identified using an enzyme-linked immunosorbent assay, immunohistochemistry, and immunofluorescence. High-throughput sequencing (HTS) was employed to identify differentially expressed genes between ADSC-Exos and ADSC-HExos. The results showed that treatment with ADSC-Exos, especially ADSC-HExos, inhibited SS-induced expression of inflammatory factors, ferroptosis, and deposition of reactive oxygen species. Results The results of HTS and polymerase chain reaction analysis revealed that GLRX2 plays an important role in protected effects of ADSC-HExo against SS-induced skin injury. In vitro analysis usingHaCaT cells confirmed that GLRX2 inhibited lipopolysaccharide-induced skin injury by inhibiting ferroptosis, as confirmed with the ferroptosis inhibitorFerrostatin-1. GLRX2 upregulation increased the therapeutic effects of ADSC-Exos against skin injury of SS mice. Conclusion Moreover,ADSC-HExos effectively promoted collagen I expression, suggesting that ADSC-HExos attenuated primary SS-induced skin injury via GLRX2 delivery and ferroptosis suppression.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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