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肥胖母亲子代的线粒体功能障碍及其通过受损卵母细胞线粒体的传递:机制的整合。

Mitochondrial dysfunction in the offspring of obese mothers and it's transmission through damaged oocyte mitochondria: Integration of mechanisms.

机构信息

Dirección de Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", México.

Hospital General de México, México.

出版信息

Biochim Biophys Acta Mol Basis Dis. 2023 Oct;1869(7):166802. doi: 10.1016/j.bbadis.2023.166802. Epub 2023 Jul 5.

DOI:10.1016/j.bbadis.2023.166802
PMID:37414229
Abstract

In vivo and in vitro studies demonstrate that mitochondria in the oocyte, are susceptible to damage by suboptimal pre/pregnancy conditions, such as obesity. These suboptimal conditions have been shown to induce mitochondrial dysfunction (MD) in multiple tissues of the offspring, suggesting that mitochondria of oocytes that pass from mother to offspring, can carry information that can programme mitochondrial and metabolic dysfunction of the next generation. They also suggest that transmission of MD could increase the risk of obesity and other metabolic diseases in the population inter- and trans-generationally. In this review, we examined whether MD observed in offspring tissues of high energetic demand, is the result of the transmission of damaged mitochondria from the oocytes of obese mothers to the offspring. The contribution of genome-independent mechanisms (namely mitophagy) in this transmission were also explored. Finally, potential interventions aimed at improving oocyte/embryo health were investigated, to see if they may provide an opportunity to halter the generational effects of MD.

摘要

体内和体外研究表明,卵母细胞中的线粒体容易受到不理想的孕前/孕期条件(如肥胖)的损害。这些不理想的条件已被证明会导致后代多个组织中的线粒体功能障碍(MD),这表明从母亲传给后代的卵母细胞中的线粒体可以携带信息,从而使下一代的线粒体和代谢功能发生编程障碍。它们还表明,MD 的传播可能会增加肥胖和其他代谢疾病在人群中跨代际的风险。在这篇综述中,我们研究了高能量需求的后代组织中观察到的 MD 是否是肥胖母亲的卵母细胞中受损线粒体传递给后代的结果。还探讨了这种传递中与基因组无关的机制(即线粒体自噬)的贡献。最后,还研究了潜在的干预措施,旨在改善卵母细胞/胚胎健康,以观察它们是否有机会阻止 MD 的代际影响。

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