ArticleStem cell research & therapy2025
Inhibition of Galectin-3 by ADSC-derived exosomes after cavernous nerve injury ameliorates erectile dysfunction by modulating oxidative stress and inflammatory profibrotic cascades.
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Extracellular vesicles in erectile dysfunction: a narrative review of multicellular regulation.Translational andrology and urology · 2026Review
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Erectile dysfunction and Peyronie's disease: from biologics to nanomedicine-enabled therapies.Sexual medicine · 2026Review
- Mechanisms of dyslipidemia-induced erectile dysfunction: a narrative review.Frontiers in endocrinology · 2026Review
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6 authors.
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Abstract
backgroundCavernous 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.
methodsWe 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.
resultsOur 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/MyD88/NF-κB signaling pathway. Following lentiviral knockdown of Gal-3, erectile function in BCNI rats was improved. Moreover, ADSC-Exo transplantation inhibited Gal-3 expression and the related inflammatory profibrotic cascades.
conclusionsCollectively, this study demonstrates that upregulation of Gal-3 promotes the pathogenesis of CNI-ED by triggering oxidative stress and inflammatory profibrotic cascades and highlights the therapeutic potential of ADSC-Exo in restoring erectile function via Gal-3 inhibition.
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