Abstract:

Polycystic ovary syndrome (PCOS), a prevalent reproductive endocrine and metabolic disorder among women of reproductive age, is characterized by ovulatory dysfunction, androgen excess, polycystic ovarian morphology, and the elevated level of serum anti-Müllerian hormone (AMH). PCOS exhibits a notable familial aggregation and genetic predisposition. The pathogenesis of PCOS is complex and multifactorial, which is currently believed to result from the combined effects of genetic and environmental factors. Recent animal experiments have demonstrated that the prenatal exposure to elevated androgen or AMH can induce a PCOS-like phenotype. Furthermore, the second filial offspring of exposed animals also display the reproductive endocrine and metabolic phenotypes associated with PCOS, confirming the transgenerational inheritance effect of PCOS. Concurrently, dietary modification or targeting the AMH signaling pathway has been shown to effectively mitigate this transgenerational inheritance of PCOS. These findings provide new insights for elucidating the pathogenesis of PCOS and reveal potential novel therapeutic targets. In this paper, we systematically review the research progress on the transgenerational inheritance of PCOS, genetic patterns, epigenetic regulatory mechanisms, and clinical evidence. Furthermore, we analyze the limitations of current research in this field.

Key words: Polycystic ovary syndrome, Heredity, Epigenesis, genetic, Androgens, Transgenerational inheritance