切换至 "中华医学电子期刊资源库"
综述

子宫内膜异位症发病机制的研究进展

  • 成萍
展开
  • 1. 524000 广东省湛江市,广东医学院
    2. 516000 广东省惠州市中心人民医院妇科
通信作者:纪燕琴,Email:
成萍,纪燕琴.子宫内膜异位症发病机制的研究进展[J/CD].中华妇幼临床医学杂志:电子版,2015,11(1):121-123.

收稿日期: 2014-11-07

  修回日期: 2014-12-10

  网络出版日期: 2015-02-01

Research progress of the pathogenesis of endometriosis

  • Ping Cheng
Expand
  • 1. Guangdong Medical College, Zhanjiang 524000, Guangdong Province, China
    2. Department of Gynecology, Huizhou Municipal Central Hospital, Huizhou 516000, Guangdong Province, China
Corresponding author: Ji Yanqin, Email:

Received date: 2014-11-07

  Revised date: 2014-12-10

  Online published: 2015-02-01

摘要

子宫内膜异位症(EM)是指具有生长功能的子宫内膜组织出现在子宫腔被覆内膜及子宫体肌层以外的其他部位,是育龄期妇女的常见疾病。目前EM的发病机制尚未明确,可能与子宫内膜干细胞、甾体类激素及其受体、新生血管生成、炎症与免疫等因素有关。笔者拟就EM发病机制的研究进展进行综述如下。

本文引用格式

成萍 . 子宫内膜异位症发病机制的研究进展[J]. 中华妇幼临床医学杂志(电子版), 2015 , 11(01) : 121 -123 . DOI: 10.3877/cma.j.issn.1673-5250.2015.01.029

Abstract

Endometriosis(EM) is defined as the presence of endometrial glands, stroma outside of the endometrial lining and uterine musculature. EM is a common gynecologic disorder among women of reproductive age. Its pathogenesis remains not clear. Current studies suggest that endometrial stem cell, steroid hormones and its veceptors, genetic factors, neovascularization, inflammation and immune may all play important roles in the pathogenesis of EM. In this review, the author focuses on the advance of the pathogenesis of EM.

参考文献

[1]
Rodgers PA,D'Hooghe TM,Fazleabas A, et al. Priorities for endometriosis research: recommendation from an international consensus workshop[J]. Reprod Sci, 2009, 16(4):335–346.
[2]
Hayashi A, Tanabe A, Kawabe S, et al. Dienogest increases the progesterone receptor isoform B/A ratio in patients with ovarian endometriosis [J]. J Ovarian Res,2012,5(1):31–38.
[3]
Anger DL, Foster WG. The link between environmental toxicant exposure and endometriosis[J]. Front Biosci, 2008, 13:1578–1593.
[4]
Gargett CE, Masuda H. Adult stem cells in the endometrium[J].Mol Hum Reprod,2010,16(11):818–834.
[5]
Chan RW, Ng EH, Yeung WS. Identification of cells with colonyforming activity, self-renewal capacity, and multipotency in ovarian endometriosis[J].Am J Pathol, 2011, 178(6):2832–2844.
[6]
Zhang WB, Cheng MJ, Huang YT, et al. A study in vitro on differentiation of bone marrow mesenchymal stem cells into endometrial epithelial cells in mice[J]. Eur J Obstet Gynecol Reprod Biol, 2012,160(2):185–190.
[7]
Snyder EY,Loring JF.A role for stem cell biology in the physiological and pathological aspects of aging[J].J Am Geriatr Soc,2005,53(9) : 287–291.
[8]
Forte A,Cipollaro M, Galderisi U. Genetic, epigenetic and stem cell alterations in endometriosis: new insights and potential therapeutic perspectives[J].Clin Sci,2014,126(2):123–138.
[9]
Bulun SE,Cheng YH,Yin P, et al. Progesterone resistance in endometriosis: link to failure to metabolize estradiol[J]. Mol Cell Endocrinol, 2006, 248(1-2):94–103.
[10]
Lessey BA,Lebovic DI,Taylor RN. Eutopic endometrium in women with endometriosis:ground zero for the study of implantation defects[J]. Semin Reprod Med,2013,31(2):109–124.
[11]
Vietri MT,Cioffi M,Sessa M,et al.CYP17 and CYP19 genepolymorphisms in women affected with endometriosis[J].Fertil Steril,2009,92(5):1532–1535.
[12]
Smuc T, Pucelj MR, Sinkovec J,et al. Expression analysis of the genes involved in estradiol and progesterone action in human ovarian endometriosis [J].Gynecol Endocrinol, 2007, 23(2):105–111.
[13]
Kitawaki J,Noguchi T.Expression of aromatase cytechrome P450 protein and messenger ribonucleic acid in human endometriotic and adenomyotic tissue but not in normal endometrium[J].Biol Reprod,1997,57(3):514–519.
[14]
Dassen H, Punyadeera C, Kamps R, et al. Estrogen metabolizing enzymes in endometrium and endometriosis [J]. Hum Reprod,2007,22(12): 3148–3158.
[15]
Hudelist G,Keckstein J, Czerwenka K, et al. Estrogen receptor beta and matrixmetallo proteinase 1 are coexpressed in uterine endometrium and endometriotic lesions of patients with endometriosis[J]. Fertil Steril,2005,84(2):1249–1256.
[16]
Trukhacheva E,Lin Z,Reierstad S,et al. ERβ regulates ERα expression in stromal cells derived from ovarian endometriosis[J].J Clin Endocrinol Metab,2009,94(2):615–622.
[17]
Gentilini D,Vigano P,Vignali M,et al. Endometrial stromal progesterone receptor A/progesterone receptor B ratio: no difference between women with and without endometriosis[J]. Fertil Steril, 2010, 94(4):1538–1540.
[18]
郎景和.子宫内膜异位症研究的新里程[J].中华妇产科杂志,2005,40(1):3–4.
[19]
Park JS,Lee JH,Kim M,et al.Endometrium from women with endometriosis shows increased proliferation activity[J]. Fertil Steril, 2009, 92(4):1246–1249.
[20]
Hapangama DK, Turner MA, Drury JA, et al. Sustained replication in endometrium of women with endometriosis occurs without evoking a DNA damage response[J].Hum Reprod,2009,24(3): 687–696.
[21]
王姝,郎景和.EM患者在位内膜特性研究新进展[J].中华妇产科杂志,2012,47(11):868–872.
[22]
Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis[J]. Fertil Steril, 2012,98(3):511–519.
[23]
Grund EM, Kagan D, Tran CA, et al. Tumor necrosis factor alpha regulates inflammatory and mesenchymal responses via mitogen-activated protein kinase,p38,and nuclear factor kappa B in human endometriotic epithelial cells[J].Mol Pharmacol, 2008, 73(5):1394–1404.
[24]
Cho S,Choi YS,Jeon YE,et al.Expression of vascular endothelial gowth factor(VEGF)and its soluble receptor-l in endometriosis[J].Microvasc Res,2012,83(2):237–242.
[25]
Abraham F, Sacerdoti F, De Lenón R,et al. Angiotensin Ⅱ activates the calcineurin/NFAT signaling pathway and induces cyclooxygenase-2 expression in rat endometrial stromal cells[J]. PLoS One,2012,7(5):e37750.
[26]
Berbic M, Fraser IS. Regulatory T cells and other leukocytes in the pathogenesis of endometriosis[J]. J Reprod Immunol, 2011,88(2):149–155.
[27]
Sikora J, Mielczarek-Palacz A, Kondera-Anasz Z.Role of natural killer cell activity in the pathogenesis of endometriosis[J].Curr Med Chem, 2011,18(2):200–208.
文章导航

/


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?