Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by irregular menstrual cycles, hyperandrogenism and subfertility. Due to its complex manifestation, the pathogenic mechanism of PCOS is not well defined. Cumulative effect of altered genetic and epigenetic factors along with environmental factors may play a role in the manifestation of PCOS leading to systemic malfunction. With failure of genome-wide association study (GWAS) and other studies performed on nuclear genome to provide any clue for precise mechanism of PCOS pathogenesis, attention has been diverted to mitochondria. Mitochondrion plays an important role in cellular metabolic functions and is linked to IR. Recently, increasing reports suggest that mitochondrial dysfunction may be a contributing factor in the pathogenesis of PCOS. Hence, in this review, we have discussed mitochondrial biology in brief and emphasizes on genetic and epigenetic aspects of mitochondrial dysfunction studied in PCOS women and PCOS-like animal models. We also highlight underlying mechanism behind mitochondrial dysfunction contributing to PCOS and its related complications such as obesity, diabetes, cardiovascular diseases, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD) and cancer. Furthermore, contrasting remarks against involvement of mitochondrial dysfunction in PCOS pathophysiology have also been presented. This review enhances our understanding in relation to mitochondrial dysfunction in the etiology of PCOS and stimulates further research to explore a clear link between mitochondrial dysfunction and PCOS pathogenesis and progression. Understanding pathogenic mechanisms underlying PCOS will open new windows to develop promising therapeutic strategies against PCOS.

中文翻译：

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线粒体功能障碍：多囊卵巢综合征病理生理学中的一个新兴环节

多囊卵巢综合征（PCOS）是一种常见的内分泌疾病，其特征是月经周期不规则、雄激素过多和生育力低下。由于其表现复杂，PCOS的发病机制尚不明确。改变的遗传和表观遗传因素以及环境因素的累积效应可能在导致全身功能障碍的 PCOS 表现中发挥作用。由于全基因组关联研究 (GWAS) 和对核基因组进行的其他研究未能为 PCOS 发病机制的精确机制提供任何线索，因此注意力已转移到线粒体上。线粒体在细胞代谢功能中起着重要作用，并与 IR 相关。最近，越来越多的报道表明线粒体功能障碍可能是 PCOS 发病机制的一个促成因素。因此，在本次审查中，我们简要讨论了线粒体生物学，并强调了在 PCOS 女性和 PCOS 样动物模型中研究的线粒体功能障碍的遗传和表观遗传方面。我们还强调了导致 PCOS 及其相关并发症的线粒体功能障碍背后的潜在机制，如肥胖、糖尿病、心血管疾病、代谢综合征、非酒精性脂肪肝 (NAFLD) 和癌症。此外，还提出了反对线粒体功能障碍参与 PCOS 病理生理学的对比评论。这篇综述增强了我们对 PCOS 病因学中线粒体功能障碍的理解，并激发了进一步的研究，以探索线粒体功能障碍与 PCOS 发病机制和进展之间的明确联系。