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关键类固醇生成酶在人胎盘中的表达及相关不良妊娠结局

Expression of Key Steroidogenic Enzymes in Human Placenta and Associated Adverse Pregnancy Outcomes.

作者信息

Cao Jiasong, Wang Yixin, Wang Shuqi, Shen Yongmei, Li Wen, Wei Zhuo, Li Shanshan, Lin Qimei, Chang Ying

机构信息

Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin Central Hospital of Gynecology Obstetrics and Nankai University Affiliated Hospital of Obstetrics and Gynecology, Tianjin 300100, China.

School of Clinical Medicine, Tianjin Medical University, Tianjin 300070, China.

出版信息

Matern Fetal Med. 2023 Jul;5(3):163-172. doi: 10.1097/FM9.0000000000000167. Epub 2022 Sep 14.

Abstract

Steroid hormones, including progestagens, estrogens, androgens, corticosteroids, and their precursor cholesterol, perform essential functions in the successful establishment and maintenance of pregnancy and normal fetal development. As the core endocrine organ at the prenatal stage, the human placenta is involved in the biosynthesis, metabolism, and delivery of steroid hormones. Steroidogenic pathways are tightly regulated by placenta-intrinsic cytochrome P450 and hydroxysteroid dehydrogenase. However, the relationship between placental steroidogenic enzyme expression and adverse pregnancy outcomes is controversial. In this review, we summarize the possible upstream regulatory mechanisms of placental steroidogenic enzymes in physiologic and pathophysiologic states. We also describe the human placental barrier model and examine the potential of single-cell sequencing for evaluating the primary functions and cellular origin of steroidogenic enzymes. Finally, we examine the existing evidence for the association between placental steroidogenic enzyme dysregulation and adverse pregnancy outcomes.

摘要

甾体激素,包括孕激素、雌激素、雄激素、皮质类固醇及其前体胆固醇,在成功建立和维持妊娠以及胎儿正常发育过程中发挥着重要作用。作为产前阶段的核心内分泌器官,人胎盘参与甾体激素的生物合成、代谢和输送。甾体生成途径受到胎盘内在细胞色素P450和羟类固醇脱氢酶的严格调控。然而,胎盘甾体生成酶表达与不良妊娠结局之间的关系存在争议。在这篇综述中,我们总结了生理和病理生理状态下胎盘甾体生成酶可能的上游调控机制。我们还描述了人胎盘屏障模型,并探讨了单细胞测序在评估甾体生成酶的主要功能和细胞起源方面的潜力。最后,我们审视了胎盘甾体生成酶失调与不良妊娠结局之间关联的现有证据。

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