The Role of TGF-β in Polycystic Ovary Syndrome. (January 2014)

• Record Type: Journal Article
• Authors: Raja-Khan, Nazia; Urbanek, Margrit; Rodgers, Raymond J.; Legro, Richard S.
• Is Part Of: Reproductive sciences. Volume 21:Number 1(2014:Jan.)
• Page Start: 20
• Page End: 31
• Publication Date: 2014-01
• Subjects: polycystic ovary syndrome -- TGF-β -- fibrillin -- genetics -- fetal origins; Reproductive health -- Periodicals; Reproduction -- Periodicals; 612.6
• DOI: 10.1177/1933719113485294
• Languages: English
• ISSNs: 1933-7191

Abstract

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 β (TGF-β) signaling. Therefore, variations in fibrillin 3 and subsequent dysregulation of TGF-β may contribute to the pathogenesis of PCOS. Here, we review the evidence from genetic studies supporting the role of TGF-β in PCOS and describe how TGF-β dysregulation may contribute to (1) the fetal origins of PCOS, (2) reproductive abnormalities in PCOS, and (3) cardiovascular and metabolic abnormalities in PCOS.