ArticleReproductive sciences (Thousand Oaks, Calif.)2025
Role of Defense/Immunity Proteins in Non-Obstructive Azoospermia: Insights from Gene Expression and Single-Cell RNA Sequencing Analyses.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Clinical and demographic characteristics of male patients with Brucellar epididymo-orchitis: a retrospective cohort study from an endemic region.Frontiers in microbiology · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-obstructive azoospermia (NOA) is a severe form of male infertility characterized by a complete absence of sperm in the ejaculate due to impaired spermatogenesis. While genetic and hormonal factors are known contributors, recent evidence highlights the role of immune dysregulation in NOA pathophysiology. Defense/immunity proteins play a crucial role in maintaining testicular immune homeostasis, but their aberrant expression may contribute to spermatogenic failure. This study analyzed gene expression data from multiple datasets to identify immune-related genes significantly altered in NOA, including IFITM1, CES1, MR1, LSAMP, PRB2, CARD8, and PECAM1. Differential expression analysis revealed upregulation of IFITM1 and PECAM1 and downregulation of CES1, MR1, LSAMP, PRB2, and CARD8, suggesting immune imbalance and oxidative stress contribute to NOA pathogenesis. Additionally, single-cell RNA sequencing confirmed their differential expression in distinct testicular cell populations. Our findings suggest that immune-related pathways, including cytokine signaling, antigen processing, and oxidative stress response, may contribute to NOA pathogenesis. Targeting these molecular pathways could provide novel therapeutic strategies for improving reproductive outcomes in affected individuals.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.