This study aimed to investigate the role of mitochondrial-related protein Mfn2 in polycystic ovary syndrome (PCOS) and its impact on oocyte development. The pathological features of PCOS model mice were confirmed by hematoxylin–eosin staining and immunohistochemistry. The expression of Mfn2 and mitochondrial-related proteins in PCOS oocytes and granulosa cells was detected by qRT-PCR and Western blot. Mitochondrial quantity was measured by Mito-Tracker staining, and the structure of mitochondria-associated ER membranes (MAMs) was observed by transmission electron microscopy. The results showed that Mfn2 was significantly downregulated in PCOS oocytes and granulosa cells, and its expression was inhibited in oocytes at different developmental stages. Moreover, the structure of MAMs was also disrupted. Downregulation of Mfn2 expression led to a reduction in mitochondrial quantity in oocytes and granulosa cells, as well as disruption of MAM structure, while overexpression of Mfn2 had the opposite effect. In conclusion, this study indicates that Mfn2 affects the development of PCOS oocytes by regulating MAMs and may be involved in maintaining the stability of MAM structure and function, thereby affecting mitochondrial quantity and function. These findings provide new insights into the pathogenesis and treatment of PCOS.

本研究旨在探讨线粒体相关蛋白Mfn2在多囊卵巢综合征（PCOS）中的作用及其对卵母细胞发育的影响。通过苏木精-伊红染色和免疫组化证实PCOS模型小鼠的病理学特征。通过qRT-PCR和Western blot检测PCOS卵母细胞和颗粒细胞中Mfn2和线粒体相关蛋白的表达。通过 Mito-Tracker 染色测量线粒体数量，并通过透射电子显微镜观察线粒体相关 ER 膜 (MAM) 的结构。结果显示，Mfn2在PCOS卵母细胞和颗粒细胞中显着下调，且其表达在不同发育阶段的卵母细胞中均受到抑制。此外，MAM的结构也被破坏。Mfn2表达下调导致卵母细胞和颗粒细胞中线粒体数量减少，以及MAM结构破坏，而Mfn2过度表达则产生相反的效果。总之，本研究表明Mfn2通过调节MAM影响PCOS卵母细胞的发育，并可能参与维持MAM结构和功能的稳定性，从而影响线粒体的数量和功能。这些发现为多囊卵巢综合症的发病机制和治疗提供了新的见解。