AKT1 和 MAPK8:妊娠糖尿病的新靶点?

IF 0.7 4区 医学 Q4 PATHOLOGY
Aysegul Turkyilmaz, Melike Nur Akin, Burcu Kasap, Cilem Ozdemİr, Aysegul Demirtas Bilgic, Tuba Gokdogan Edgunlu
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引用次数: 0

摘要

目的:妊娠糖尿病(GDM)会破坏胎盘功能并增加妊娠风险。本研究探讨了 AKT1 和 MAPK8 基因在胰岛素抵抗和细胞信号传导中的潜在作用。研究方法使用实时 PCR 分析 GDM 患者和健康对照组的胎盘组织,量化基因表达水平。硅学分析进一步探讨了表达变化的功能意义。结果发现与对照组相比,GDM 胎盘中 AKT1 和 MAPK8 的表达发生了显著变化(分别为 p = 0.047 和 p = 0.007)。硅学分析表明潜在的功能性后果与糖尿病相关通路有关。结论本研究确定了 AKT1 和 MAPK8 在 GDM 胎盘中的不同表达,表明它们在疾病过程中的潜在作用。进一步研究它们的功能贡献可为 GDM 病理生理学和潜在治疗靶点提供有价值的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
AKT1 and MAPK8: New Targets for Gestational Diabetes Mellitus?

Objective: Gestational diabetes mellitus (GDM) disrupts placental function and increases risks for pregnancy. This study investigates the potential involvement of AKT1 and MAPK8 genes, known for their roles in insulin resistance and cell signaling, in GDM pathophysiology. Methods: Placental tissues from GDM patients and healthy controls were analyzed using real-time PCR to quantify gene expression levels. In silico analysis further explored the functional implications of expression changes. Results: AKT1 and MAPK8 displayed significantly altered expression in GDM placentas compared to controls (p = 0.047 and p = 0.007, respectively). In silico analysis suggests potential functional consequences related to diabetes-associated pathways. Conclusion: This study identifies differential expression of AKT1 and MAPK8 in GDM placentas, suggesting their potential roles in the disease process. Further investigation into their functional contributions could provide valuable insights into GDM pathophysiology and potential therapeutic targets.

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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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