ArticleFrontiers in cell and developmental biology2026
A multi-mics exploration of programmed cell death in non-obstructive azoospermia: identifying TLR4 as a central regulator and therapeutic target.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Differential expression of ALOX15 and GPX4 in the testicular tissue of men with obstructive and non-obstructive azoospermia: a cross-sectional study.Translational andrology and urology · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Male infertility (MI) is a globally recognized public health challenge, affecting approximately 18% of men of reproductive age worldwide. Non-obstructive azoospermia (NOA) is a major cause of NOA and is associated with dysregulated programmed cell death (PCD). However, the precise role and mechanisms of PCD in the pathogenesis of NOA remain poorly understood. Methods: In this study, target genes associated with both PCD and NOA were retrieved from multiple public databases. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were then performed to explore underlying mechanisms. Subsequently, protein-protein interaction (PPI) network analysis identified hub genes within the network. Mendelian randomization (MR) analysis was further conducted to establish a causal relationship between key genes and NOA susceptibility. Thereafter, Results: Our analysis identified 150 PCD-related genes that were dysregulated in NOA. GO and KEGG enrichment analyses indicated that these targets primarily regulate cell death, senescence, inflammation, oxidative stress, and various biosynthetic processes. PPI analysis identified 10 hub genes: HIF1A, TLR4, MDM2, GPX4, SNCA, MTOR, CSNK2A2, ATG5, CTSS, and PIK3CA. Subsequent MR analysis established TLR4 as being causally associated with an increased risk of NOA. Conclusion: This study advances the understanding of PCD in the pathogenesis of NOA. It identifies and underscores the critical role of the core PCD-related gene TLR4 in NOA development, highlighting the necessity for strategies aimed at mitigating its negative impact on fertility.
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