Inhibition of Galectin-3 by ADSC-derived exosomes after cavernous nerve injury ameliorates erectile dysfunction by modulating oxidative stress and inflammatory profibrotic cascades.
Li R., Wang G., Feng C., Diao T., Liu S., Fu Q.
Animal Study, published in Stem Cell Res Ther (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
- Stem Cell Res Ther (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41204281
- DOI
- 10.1186/s13287-025-04749-w
Abstract (original English)
Cavernous nerve injury (CNI) is a prominent etiological factor in the development of erectile dysfunction (ED). Nevertheless, the underlying pathophysiological mechanisms of CNI-induced ED (CNI-ED) are not fully elucidated. Galectin-3 (Gal-3), an indicator of inflammation and fibrosis, has been implicated in the pathogenesis of arteriogenic ED. In this study, we investigate the role of Gal-3 in CNI-ED and explore the potential mechanisms by which adipose-derived mesenchymal stem cell exosomes (ADSC-Exo) ameliorate CNI-ED. We established a bilateral CNI (BCNI) rat model and evaluated erectile function using intracavernous pressure (ICP), mean arterial pressure (MAP), and infrared ray thermography (IRT). The expression level of Gal-3 was measured in the major pelvic ganglia (MPG), penile corpus cavernosum, and cultured cells, with its expression modulated by lentiviral vectors. A combination of experimental approaches, including western blot, immunofluorescence, and flow cytometry analysis, were employed to investigate the role of Gal-3 in the progression of CNI-ED. Additionally, the potential molecular mechanisms by which ADSC-Exo ameliorates CNI-ED were explored. Our findings indicated that the expression of Gal-3 is significantly upregulated in the MPG and penile corpus cavernosum of BCNI rats. This upregulation was accompanied by oxidative stress and activation of the TLR4/My
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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