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本文引用的文献

1
Complement and the Regulation of T Cell Responses.补体系统与 T 细胞应答的调节。
Annu Rev Immunol. 2018 Apr 26;36:309-338. doi: 10.1146/annurev-immunol-042617-053245.
2
Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia.补体 5a 介导体滋养层细胞功能障碍与子痫前期的发生有关。
J Cell Mol Med. 2018 Feb;22(2):1034-1046. doi: 10.1111/jcmm.13466. Epub 2017 Nov 23.
3
Novel mechanisms and functions of complement.补体的新机制与功能
Nat Immunol. 2017 Nov 16;18(12):1288-1298. doi: 10.1038/ni.3858.
4
The complement system is dysfunctional in metabolic disease: Evidences in plasma and adipose tissue from obese and insulin resistant subjects.补体系统在代谢性疾病中功能失调:肥胖和胰岛素抵抗患者的血浆和脂肪组织中的证据。
Semin Cell Dev Biol. 2019 Jan;85:164-172. doi: 10.1016/j.semcdb.2017.10.025. Epub 2017 Oct 28.
5
The Complement System and Preeclampsia.补体系统与子痫前期。
Curr Hypertens Rep. 2017 Oct 18;19(11):87. doi: 10.1007/s11906-017-0784-4.
6
Analysis of Complement Gene Reveals Susceptibility to Severe Preeclampsia.补体基因分析揭示重度子痫前期易感性。
Front Immunol. 2017 May 29;8:589. doi: 10.3389/fimmu.2017.00589. eCollection 2017.
7
Relationships between Rodent White Adipose Fat Pads and Human White Adipose Fat Depots.啮齿动物白色脂肪垫与人类白色脂肪储存部位之间的关系。
Front Nutr. 2016 Apr 19;3:10. doi: 10.3389/fnut.2016.00010. eCollection 2016.
8
Clinical risk factors for pre-eclampsia determined in early pregnancy: systematic review and meta-analysis of large cohort studies.孕早期确定的子痫前期临床危险因素:大型队列研究的系统评价和荟萃分析
BMJ. 2016 Apr 19;353:i1753. doi: 10.1136/bmj.i1753.
9
Hypertensive Disorders of Pregnancy.妊娠高血压疾病
Am Fam Physician. 2016 Jan 15;93(2):121-7.
10
Immune Mechanisms Linking Obesity and Preeclampsia.连接肥胖与子痫前期的免疫机制
Biomolecules. 2015 Nov 12;5(4):3142-76. doi: 10.3390/biom5043142.

肥胖“补充”子痫前期。

Obesity "complements" preeclampsia.

机构信息

Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University , Baton Rouge, Louisiana.

Reproductive Endocrinology & Women's Health Lab, Pennington Biomedical Research Center , Baton Rouge, Louisiana.

出版信息

Physiol Genomics. 2019 Mar 1;51(3):73-76. doi: 10.1152/physiolgenomics.00102.2018. Epub 2019 Feb 4.

DOI:10.1152/physiolgenomics.00102.2018
PMID:30716010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6459374/
Abstract

Preeclampsia (PE) is a devastating adverse outcome of pregnancy. Characterized by maternal hypertension, PE, when left untreated, can result in death of both mother and baby. The cause of PE remains unknown, and there is no way to predict which women will develop PE during pregnancy. The only known treatment is delivery of both the fetus and placenta; therefore, an abnormal placenta is thought to play a causal role. Women with obesity before pregnancy have an increased chance of developing PE. Increased adiposity results in a heightened state of systemic inflammation that can influence placental development. Adipose tissue is a rich source of proinflammatory cytokines and complement proteins, which have been implicated in the pathogenesis of PE by promoting the expression of antiangiogenic factors in the mother. Because an aggravated inflammatory response, angiogenic imbalance, and abnormal placentation are observed in PE, we hypothesize that maternal obesity and complement proteins derived from adipose tissue play an important role in the development of PE.

摘要

子痫前期 (PE) 是妊娠的一种严重不良结局。其特征为母体高血压,如果不加以治疗,可能会导致母婴死亡。PE 的病因仍不清楚,也无法预测哪些女性在怀孕期间会患上 PE。唯一已知的治疗方法是分娩胎儿和胎盘;因此,异常胎盘被认为起着因果关系。孕前肥胖的女性患 PE 的几率增加。肥胖会导致全身性炎症状态加剧,从而影响胎盘发育。脂肪组织是促炎细胞因子和补体蛋白的丰富来源,这些细胞因子和蛋白通过在母体中促进抗血管生成因子的表达,参与了 PE 的发病机制。由于在 PE 中观察到炎症反应加剧、血管生成失衡和胎盘异常,我们假设母体肥胖和来自脂肪组织的补体蛋白在 PE 的发展中起着重要作用。