ArticleBMC medical genomics2022
Bioinformatics analysis identifies potential hub genes and crucial pathways in the pathogenesis of asthenozoospermia.
Article in BMC medical genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- DCDC2C Protein Expression in Human Spermatozoa: A Potential Molecular Marker for Asthenozoospermia.Medical sciences (Basel, Switzerland) · 2026Article
- Association of EEF1A1 and linc00993 expression with sperm morphology in teratozoospermia: an integrative in silico and in vitro study.Scientific reports · 2026Article
- Semenogelin I-derived peptide SgI-52 binds membrane Peroxiredoxin 6 and induces oxidative stress in asthenozoospermic sperm.Reproductive biology and endocrinology : RB&E · 2025Article
- ANKEF1 is a key axonemal component essential for murine sperm motility and male fertility.eLife · 2025Article
- Identification and validation of immune and diagnostic biomarkers for interstitial cystitis/painful bladder syndrome by integrating bioinformatics and machine-learning.Frontiers in immunology · 2025Article
- Comparison of different processed products ofTranslational andrology and urology · 2024Article
- Identification of potential biomarkers and pathways for asthenozoospermia by bioinformatics analysis and experiments.Frontiers in endocrinology · 2024Article
- Elucidation of the mechanism of action of ailanthone in the treatment of colorectal cancer: integration of network pharmacology, bioinformatics analysis and experimental validation.Frontiers in pharmacology · 2024Article
- The construction of a testis transcriptional cell atlas from embryo to adult reveals various somatic cells and their molecular roles.Journal of translational medicine · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthenozoospermia is a troublesome disease experienced by men in their reproductive years, but its exact etiology remains unclear. To address this problem, this study aims to identify the hub genes and crucial pathways in asthenozoospermia.
methodsWe screened two Gene Expression Omnibus (GEO) datasets (GSE92578 and GSE22331) to extract the differentially expressed genes (DEGs) between normozoospermic and asthenozoospermic men using the "Limma" package. Gene enrichment analyses of the DEGs were conducted using the "clusterProfiler" R package. The protein-protein interaction (PPI) network was then established using the STRING database. A miRNA-transcription factor-gene network was constructed based on the predicted results of hub genes using the RegNetwork database. The expression of four hub genes in asthenozoospermia and normal samples were verified using quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting.
resultsWe identified 271 DEGs, which included 218 upregulated and 53 downregulated in two asthenozoospermia datasets. These DEGs were observed to be markedly enriched in pathways with cell growth and embryonic organ development, phospholipase D signaling pathway, cGMP-PKG signaling pathway, and Wnt signaling pathway. The most significant genes were identified, including COPS7A, CUL3, KLHL7, NEDD4. We then constructed regulatory networks of these genes, miRNAs, and transcription factors. Finally, we found that the COPS7A was significantly upregulated in patients with asthenozoospermia, but CUL3, KLHL7 and NEDD4 were significantly downregulated compared with normal samples.
conclusionWe applied bioinformatics methods to analyze the DEGs of asthenozoospermia based on the GEO database and identified the novel crucial genes and pathways in this disease. Our findings may provide novel insights into asthenozoospermia and identify new clues for the potential treatment of this disease.
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