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This study investigates autophagy and apoptosis in PBMCs of patients with endometrial atrophy, suggesting possible pathways.
Abstract Introduction: Endometrial atrophy (EA) is a disease in which the endometrium becomes very thin, so that its thickness never reaches more than 5 mm. In most cases, the origin of EA is not known, but factors can cause thinning of the endometrium, including contraceptive drugs, inflammatory, iatrogenic, and in some cases, hereditary factors. Autophagy has an important consequence in the proper functioning of the uterus, reproductive physiology and endometrial atrophy.Method: In this study, Real-Time PCR was used to measure the expression levels of autophagy genes ATG5, ATG7, LC3B, Beclin1, FOXO1, FOXO3a, FOXO4 and FOXO6 in 40 women with thin endometrium and 40 healthy pregnant women. In addition to, apoptosis was done by flow cytometry method.Results: Evaluation of the expression level of autophagy genes showed a significant difference in studied groups, so that the expression levels of ATG5, ATG7 and LC3B, Beclin1, FOXO1, FOXO3a, FOXO4 and FOXO6 genes were higher in the patient group. Moreover, there was a positive correlation between the expression of autophagy gene LC3B and the frequency of apoptotic cells in the studied patients.Disscusion: To further elucidate the biological pathways and processes associated with the differentially expressed autophagy genes, we conducted a KEGG pathway enrichment analysis using the EnrichR tool. Our results showed that autophagy genes with apoptosis in PBMC cells may be involved in endometrial thinning of EA patients.
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kalkhoran et al. (2025) studied this question.
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