Integrative bioinformatics analysis of lipid metabolism-related genes and immune infiltration in endometriosis
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Abstract
Endometriosis is referred to as a "benign cancer," severely impacting women's reproductive health. However, the pathogenesis of endometriosis remains unclear. This study aims to investigate the potential roles of lipid metabolism-related genes (LMRGs) and immune infiltration in the diagnosis and pathogenesis of endometriosis. Four microarray datasets (GSE6364, GSE51981, GSE153740, and GSE232713) with eutopic endometrium samples of the midsecretory phase were downloaded from the Gene Expression Omnibus database. Seven hundred forty LMRGs were obtained from the Reactome database. The GSE6364 and GSE51981 datasets were merged and differentially expressed genes (DEGs) were identified between endometriosis patients and normal controls. Lipid metabolism-related DEGs were detected by intersecting the DEGs and LMRGs. Functional enrichment analysis, protein-protein interaction analysis, and receiver operating characteristic analysis of lipid metabolism-related DEGs were performed. Additionally, immune cell infiltration was compared between endometriosis patients and normal controls, and associations with lipid metabolism-related DEGs were assessed. Fifty-eight lipid metabolism-related DEGs were identified in endometriosis patients compared with normal controls, which enriched in glycerolipids, fatty acyls, sphingolipids, glycerophospholipids, and sterol lipids metabolism, especially steroid hormone metabolism and arachidonic acid metabolism. Additionally, 11 core genes were identified, with HMGCR and CYP27A1 validated as potential markers for diagnosing endometriosis and assessing its severity, respectively. Immune infiltration analysis revealed that fibroblasts and B lineage cells were predominantly abnormal in the endometrium of the midsecretory phase in endometriosis. Correlation analysis suggested that core genes were closely related to immune cells. In conclusion, HMGCR and CYP27A1 were identified as potential markers for endometriosis and its severity, respectively. Fibroblasts and B lineage cells may significantly contribute to the reduced endometrial receptivity observed in endometriosis. These findings provide new insights into the diagnostic and pathogenic roles of LMRGs in endometriosis and highlight their implications for infertility and pregnancy complications related to endometriosis.
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References (55)
- A Case Exemplifying Sampson's Theory of the Aetiology of Endometriosis via openalex
- Causal association of immune cells and endometriosis: a Mendelian randomization study via openalex
- Effect of simvastatin on baboon endometriosis† via openalex
- Emerging hallmarks of endometriosis metabolism: A promising target for the treatment of endometriosis via openalex
- Endometrial causes of recurrent pregnancy losses: endometriosis, adenomyosis, and chronic endometritis via openalex
- Endometriosis and infertility: pathophysiology and management via openalex
- Endometriosis and obstetrics complications: a systematic review and meta-analysis via openalex
- Endometriosis: Cellular and Molecular Mechanisms Leading to Fibrosis via openalex
- Endometriosis recurrence following post-operative hormonal suppression: a systematic review and meta-analysis via openalex
- Epigenetic Factors in Eutopic Endometrium in Women with Endometriosis and Infertility via openalex
- Expression of HOXA10 Gene in Women with Endometriosis: A Systematic Review via openalex
- Human Endometrial Fibroblasts Derived from Mesenchymal Progenitors Inherit Progesterone Resistance and Acquire an Inflammatory Phenotype in the Endometrial Niche in Endometriosis1 via openalex
- Is the profile of transcripts altered in the eutopic endometrium of infertile women with endometriosis during the implantation window? via openalex
- Lipophilic statins inhibit growth and reduce invasiveness of human endometrial stromal cells via openalex
- Pathogenesis of Endometriosis: New Insights into Prospective Therapies via openalex
- Polymorphisms and endometriosis: a systematic review and meta-analyses via openalex
- Role of Eutopic Endometrium in Pelvic Endometriosis via openalex
- Single-cell transcriptomic analysis of endometriosis provides insights into fibroblast fates and immune cell heterogeneity via openalex
- The effects of Rituximab on experimental endometriosis model in rats via openalex
- The estrogen-regulated lncRNA H19/miR-216a-5p axis alters stromal cell invasion and migration via ACTA2 in endometriosis via openalex
- The inhibitory effect of celecoxib and rosiglitazone on experimental endometriosis via openalex
- The involvement of RNA N6-methyladenosine and histone methylation modification in decidualization and endometriosis-associated infertility via openalex
- The molecular connections between the cannabinoid system and endometriosis via openalex
- Therapeutic Roles of Statins in Gynecology and Obstetrics: The Current Evidence via openalex
- The role of peroxisome proliferator-activated receptors in endometriosis via openalex
- The role of the B lymphocytes in endometriosis: A systematic review via openalex
- W4388539829 via openalex
- W4392579064 via openalex
- W1503157502 via openalex
- W6752006146 via openalex
- W1859798930 via openalex
- W1953845294 via openalex
- W2003081211 via openalex
- W2027924835 via openalex
- W2045079381 via openalex
- W2101386379 via openalex
- W2107665951 via openalex
- W2114220878 via openalex
- W2119615715 via openalex
- W2131644380 via openalex
- W2170134016 via openalex
- W2204640292 via openalex
- W2533508881 via openalex
- W2805393256 via openalex
- W2810127666 via openalex
- W2888563275 via openalex
- W3134885188 via openalex
- W3164100141 via openalex
- W4200358505 via openalex
- W4205353903 via openalex
- W4214582077 via openalex
- W4225380040 via openalex
- W4281624755 via openalex
- W4328135802 via openalex
- W4386625232 via openalex
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