C R Biol. 2024 Apr 19;347:19-25. doi: 10.5802/crbiol.147.
Polycystic ovary syndrome (PCOS) is the most common endocrine and metabolic disorder in women of reproductive age. It has a strong hereditary component estimated at 60 to 70% in daughters. It has been suggested that environmental factors during the fetal period may be involved in the development of the syndrome in adulthood. However, the underlying mechanisms of its transmission remain unknown, thus limiting the development of effective therapeutic strategies.This article highlights how an altered fetal environment (prenatal exposure to high levels of anti-Müllerian hormone) can contribute to the onset of PCOS in adulthood and lead to the transgenerational transmission of neuroendocrine and metabolic traits through alterations in the DNA methylation process.The originality of the translational findings summarized here involves the identification of potential biomarkers for early diagnosis of the syndrome, in addition to the validation of a promising therapeutic avenue in a preclinical model of PCOS, which can improve the management of patients suffering from the syndrome.
多囊卵巢综合征(PCOS)是育龄妇女中最常见的内分泌和代谢紊乱疾病。据估计,其遗传性占 60%至 70%。有研究表明,胎儿期的环境因素可能与成年后患该病有关。然而,其传播的潜在机制尚不清楚,从而限制了有效治疗策略的发展。本文重点介绍了胎儿期环境改变(产前暴露于高水平抗苗勒管激素)如何导致成年后患 PCOS,并通过 DNA 甲基化过程的改变导致神经内分泌和代谢特征的跨代传递。这里总结的转化研究的创新性在于确定了用于该综合征早期诊断的潜在生物标志物,以及在 PCOS 的临床前模型中验证了一种有前途的治疗途径,这可以改善患有该综合征的患者的管理。