Mitochondrial epigenetic modifications and nuclear-mitochondrial communication: A new dimension towards understanding and attenuating the pathogenesis in women with PCOS.

Mitochondrial DNA (mtDNA) epigenetic modifications have recently gained attention in a plethora of complex diseases, including polycystic ovary syndrome (PCOS), a common cause of infertility in women of reproductive age. Herein we discussed mtDNA epigenetic modifications and their impact on nuclear-mitochondrial interactions in general and the latest advances indicating the role of mtDNA methylation in the pathophysiology of PCOS. We highlighted epigenetic changes in nuclear-related mitochondrial genes, including nuclear transcription factors that regulate mitochondrial function and may be involved in the development of PCOS or its related traits. Additionally, therapies targeting mitochondrial epigenetics, including time-restricted eating (TRE), which has been shown to have beneficial effects by improving mitochondrial function and may be mediated by epigenetic modifications, have also been discussed. As PCOS has become a major metabolic disorder and a risk factor for obesity, cardiometabolic disorders, and diabetes, lifestyle/behavior intervention using TRE that reinforces feeding-fasting rhythms without reducing caloric intake may be a promising therapeutic strategy for attenuating the pathogenesis. Furthermore, future perspectives in the area of mitochondrial epigenetics are described.

线粒体DNA（mtDNA）的表观遗传修饰最近在众多复杂疾病中受到关注，包括多囊卵巢综合征（PCOS），这是育龄女性不孕的常见原因。在此，我们讨论了mtDNA的表观遗传修饰及其对核 - 线粒体相互作用的总体影响，以及表明mtDNA甲基化在多囊卵巢综合征病理生理学中作用的最新进展。我们强调了核相关线粒体基因的表观遗传变化，包括调节线粒体功能且可能参与多囊卵巢综合征或其相关特征发展的核转录因子。此外，还讨论了针对线粒体表观遗传学的疗法，包括限时进食（TRE），它已被证明可通过改善线粒体功能产生有益效果，并且可能是由表观遗传修饰介导的。由于多囊卵巢综合征已成为一种主要的代谢紊乱，是肥胖、心脏代谢紊乱和糖尿病的风险因素，使用限时进食的生活方式/行为干预在不减少热量摄入的情况下强化进食 - 禁食节律，可能是一种有希望的减轻发病机制的治疗策略。此外，还描述了线粒体表观遗传学领域的未来展望。