Unveiling the role of galectin-3 in patients with azoospermia: potential biomarker for male infertility
ZYGOTE, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1017/s0967199426100513
- Dergi Adı: ZYGOTE
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE, Zoological Record, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Health Research Premium Collection (ProQuest)
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- İstanbul Üniversitesi Adresli: Evet
Özet
Objective: To investigate the role of the protein galectin-3 (Gal-3) and its effect on fibrosis and apoptosis in testicular tissues of patients with idiopathic non-obstructive azoospermia (iNOA).Design: A prospective study.Subject: Male patients who needed testicular sperm extraction for assisted reproductive technology treatments.Exposure: Tissue samples were obtained during microdissection testicular sperm extraction (mTESE) procedures from patients diagnosed as having azoospermia according to two semen analyses. Two groups were determined as sperm non-detected (n = 8, TESE-) and detected (n = 7, TESE+). Germ cells were morphologically evaluated using haematoxylin and eosin-stained sections and Johnsen scores. Immunohistochemical methods were used to evaluate Gal-3 expression and caspase-3-related apoptotic activity.Main outcome measures: Gal-3 positivity, apoptosis and fibrosis indexes.Results: Gal-3 expression was significantly higher in the TESE- group (p = 0.024). Gal-3 showed strong positivity in Sertoli Cells and cells in the interstitial area around the seminiferous tubules in the TESE- group.Conclusion: This study highlights the potential role of Gal-3 in iNOA and its association with testicular fibrosis and impaired spermatogenesis. The absence of sperm retrieval was associated with increased Gal-3 expression, seminiferous tubule wall thickening, and enhanced apoptosis-related activity. These findings suggest that Gal-3 may contribute to inflammation- and fibrosis-related testicular damage in iNOA. However, further experimental and clinical studies are required to clarify the underlying molecular mechanisms of Gal-3 and determine its potential clinical significance in male infertility.