Raja-Khan, N.Urbanek, M.Rodgers, R.Legro, R.2013-10-222013-10-222014Reproductive Sciences, 2014; 21(1):20-311933-71911933-7205http://hdl.handle.net/2440/80549Polycystic 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.en© The Author(s) 2013polycystic ovary syndromeTGF-βfibrillingeneticsfetal originsJournal article002013171010.1177/19337191134852940003279272000032-s2.0-8489028140018083Rodgers, R. [0000-0002-2139-2969]