인문학
사회과학
자연과학
공학
의약학
농수해양학
예술체육학
복합학
개인구독
소속 기관이 없으신 경우, 개인 정기구독을 하시면 저렴하게
논문을 무제한 열람 이용할 수 있어요.
지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록·키워드
Abstract Background Recurrent embryo implantation failure (RIF) poses a considerable obstacle in the management of in vitro fertilization (IVF), as IVF failure has been linked to the presence of endometriosis, the growth of endometrial-like tissue outside the uterus. Therefore, this study aimed to reveal the molecular mechanisms connecting endometriosis and RIF, offering valuable knowledge on potential therapeutic targets and biomarkers. Methods A comprehensive investigation was conducted on gene expression data from the GEO database, focusing on three datasets related to endometriosis and RIF, which revealed distinct gene expression patterns and facilitated functional enrichment analysis to identify significant biological processes and molecular pathways associated with these differentially expressed genes. Protein–protein interaction networks were also established to identify critical genes. Results A total of 43 differentially expressed genes (DEGs) were identified, shared between endometriosis and RIF, with enrichment analysis highlighting pathways related to interleukin-6 signaling, FOXO-mediated transcription, smooth muscle contraction, and semaphorin interactions. Gene ontology studies revealed the significance of signal transduction and apoptosis regulation. ESR1, SOCS3, MYH11, CYP11A1, and CLU were identified as hub genes with potential as therapeutic targets and diagnostic indicators. Conclusion This study advances our understanding of the molecular framework underlying endometriosis and RIF. This presents potential possibilities for tailored treatment approaches and enhanced therapeutic results for individuals experiencing repeated or severe reproductive difficulties.
인공지능 문자 인식 모델을 통해 추출된 텍스트로, 일부 오타나 오류가 포함될 수 있으나 지속적으로 개선 중입니다.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.
오류를 발견하셨다면 해당 부분을 드래그한 후 ' 를 통해 신고해주세요.