Abstract
One contributing factor to the pathophysiology of hyperandrogenemia associated with PCOS is an intrinsic alteration in ovarian steroidogenesis, leading to enhanced synthesis of androgens including testosterone (T). Increased activity of CYP17A1, the rate-limiting enzyme for the formation of androgens in the gonads, is thought to be a critical factor driving enhanced T secretion in PCOS. Given their diverse roles in biological process, interest has grown in the role of noncoding RNAs (ncRNAs) in the pathogenesis of PCOS.
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