AI Article Synopsis

  • Polycystic ovary syndrome (PCOS) is a widespread reproductive disorder, but its causes are poorly understood, and this study explores necroptosis, a new type of cell death linked to reproductive health issues.
  • Researchers used bioinformatics to analyze gene expression data from multiple datasets, identifying key necroptosis-related genes and their relationship with immune cell infiltration in PCOS patients.
  • The findings suggest that necroptosis-related genes play a significant role in the development of PCOS and could be connected to immune responses in these patients.

Article Abstract

Background: Polycystic ovary syndrome (PCOS) is a common reproductive and endocrine disorder; however, the understanding of the pathogenesis of PCOS remains unclear. Necroptosis is a newly discovered mechanism of cell death, and it is closely related to reproductive endocrine-related diseases. This study aimed to investigate the hub necroptosis-related genes in PCOS patients and its correlation with immune cell infiltration by bioinformatics methods.

Method: The gene expression chip result matrix and the annotation matrix files of the GSE34526, GSE8157, and GSE5090 datasets were downloaded from the GEO database. We analyzed the expression and correlation of the necroptosis-related genes in all samples, constructed a diagnostic model based on all necroptosis-related genes and genes with significant differences, performed unsupervised clustering of samples and gene enrichment analysis, and evaluated the correlations between the hub gene and immune cell infiltration levels by the R packages GSVA and CIBERSORT. Finally, PPI networks were constructed using the Cytoscape software GeneMANIA plug-in, and the miRNA, transcription factors, RBP, and drugs were predicted.

Conclusion: Necroptosis-related genes have important relationships in the development of PCOS and are potentially associated with immune infiltration in PCOS patients.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11707095PMC
http://dx.doi.org/10.1007/s10815-024-03286-4DOI Listing

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