The Role of TGF-β in Polycystic Ovary Syndrome

被引：97

作者：

Raja-Khan, Nazia ^{[1
]}

Urbanek, Margrit ^{[2
]}

Rodgers, Raymond J. ^{[3
]}

Legro, Richard S. ^{[4
]}

机构：

[1] Penn State Univ, Div Endocrinol Diabet & Metab, Coll Med, MS Hershey Med Ctr, Hershey, PA 17033 USA

[2] Northwestern Univ, Feinberg Sch Med, Div Endocrinol Metab & Mol Med, Chicago, IL 60611 USA

[3] Univ Adelaide, Res Ctr Reprod Hlth, Discipline Obstet & Gynaecol, Robinson Inst, Adelaide, SA 5005, Australia

[4] Penn State Univ, Dept Obstet & Gynecol, Coll Med, MS Hershey Med Ctr, Hershey, PA 17033 USA

来源：

REPRODUCTIVE SCIENCES | 2014年 / 21卷 / 01期

关键词：

polycystic ovary syndrome; TGF-beta; fibrillin; genetics; fetal origins; TRANSFORMING-GROWTH-FACTOR; POLYMORPHIC DINUCLEOTIDE REPEAT; REGULAR MENSTRUAL CYCLES; EXTRACELLULAR-MATRIX; BINDING-PROTEINS; FOLLISTATIN GENE; FOLLICLE DEVELOPMENT; ANDROGEN PRODUCTION; KINASE INHIBITOR; INCREASED RISK;

D O I：

10.1177/1933719113485294

中图分类号：

R71 [妇产科学];

学科分类号：

100211 ;

摘要：

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic oligoanovulation and hyperandrogenism and associated with insulin resistance, type 2 diabetes, and cardiovascular risk. In recent years, genetic studies have linked PCOS to a dinucleotide marker D19S884 in the fibrillin 3 gene. Fibrillins make up the major component of microfibrils in the extracellular matrix (ECM) and interact with molecules in the ECM to regulate transforming growth factor (TGF-beta) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-beta may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF- in PCOS and describe how TGF-beta dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.

引用

页码：20 / 31

页数：12

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