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Abstract

Volume 24, Issue 4 (July 2022) 24, 422–429; 10.4103/aja2021109

The association between mutations in ubiquitin-specific protease 26 (USP26) and male infertility: a systematic review and meta-analysis

Qin-Yu Li1, Yu-Cong Zhang2, Chao Wei1, Zhuo Liu1, Guo-Da Song1, Bing-Liang Chen1, Man Liu1, Ji-Hong Liu1, Li-Cheng Wu1, Xia-Ming Liu1

1 Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
2 Department of Geriatric, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China

Correspondence: Dr. XM Liu (xmliu77@hust.edu.cn) or Dr. LC Wu (achengge@126.com)

Date of Submission 10-Jun-2021 Date of Acceptance 22-Nov-2021 Date of Web Publication 21-Jan-2022

Abstract

During recent decades, the association between mutations in ubiquitin-specific protease 26 (USP26) and male infertility remains doubtful. We conducted this meta-analysis to evaluate the association between mutations in USP26 and male infertility according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. It was registered in the International Prospective Register of Systematic Reviews (PROSPERO; CRD42021225251). PubMed, Web of Science, and Scopus were systematically searched for comparative clinical studies, which were written in English and provided eligible data. Studies were included when they compared USP26 mutations in azoospermic, oligozoospermic, and asthenozoospermic patients with controls with normal sperm parameter values or whose partners had experienced spontaneous pregnancy. Pooled odds ratio (OR) with 95% confidence interval (CI) was calculated with random effect models. Overall, twelve studies with 3927 infertility patients and 4648 healthy controls were included. The association between overall USP26 mutations and infertility was not significant (OR = 1.60, 95% CI: 0.51–5.01). For specific mutations, the pooled ORs were 1.65 (95% CI: 1.02–2.69) for cluster mutation (including 370–371insACA, 494T>C, and 1423C>T), 1.80 (95% CI: 0.35–9.15) for c.576G>A, 1.43 (95% CI: 0.79–2.56) for c.1090C>T, and 3.59 (95% CI: 2.30–5.59) for c.1737G>A. Our results suggest that several mutations (cluster mutation, c.1737G>A) may play roles in male infertility, while others (c.576G>A and c.1090C>T) do not show notable associations with male infertility. More high-quality clinical researches are needed for validation.

Keywords: azoospermia; haplotype; male infertility; mutation; ubiquitin-specific protease 26

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