Yildirim Raziye Melike, Ergun Yagmur, Basar Murat
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT 06510, USA.
Yale Fertility Center, 200 West Campus Drive, Orange, CT 06477, USA.
Biomedicines. 2022 Oct 12;10(10):2539. doi: 10.3390/biomedicines10102539.
Mitochondria are essential organelles and crucial for cellular survival. Mitochondrial biogenesis and mitophagy are dynamic features that are essential for both maintaining the health of the mitochondrial network and cellular demands. The accumulation of damaged mitochondria has been shown to be related to a wide range of pathologies ranging from neurological to musculoskeletal. Mitophagy is the selective autophagy of mitochondria, eliminating dysfunctional mitochondria in cells by engulfment within double-membraned vesicles. Preeclampsia and low birth weight constitute prenatal complications during pregnancy and are leading causes of maternal and fetal mortality and morbidity. Both placental implantation and fetal growth require a large amount of energy, and a defect in the mitochondrial quality control mechanism may be responsible for the pathophysiology of these diseases. In this review, we compiled current studies investigating the role of BNIP3, DRAM1, and FUNDC1, mediators of receptor-mediated mitophagy, in the progression of preeclampsia and the role of mitophagy pathways in the pathophysiology of low birth weight. Recent studies have indicated that mitochondrial dysfunction and accumulation of reactive oxygen species are related to preeclampsia and low birth weight. However, due to the lack of studies in this field, the results are controversial. Therefore, mitophagy-related pathways associated with these pathologies still need to be elucidated. Mitophagy-related pathways are among the promising study targets that can reveal the pathophysiology behind preeclampsia and low birth weight.
线粒体是必不可少的细胞器，对细胞存活至关重要。线粒体生物发生和线粒体自噬是动态特征，对于维持线粒体网络的健康和细胞需求都必不可少。已表明受损线粒体的积累与从神经到肌肉骨骼等广泛的病理状况有关。线粒体自噬是线粒体的选择性自噬，通过被双膜囊泡吞噬来消除细胞中功能失调的线粒体。子痫前期和低出生体重是孕期的产前并发症，是孕产妇和胎儿死亡及发病的主要原因。胎盘植入和胎儿生长都需要大量能量，线粒体质量控制机制的缺陷可能是这些疾病病理生理的原因。在本综述中，我们汇总了当前研究，这些研究调查了受体介导的线粒体自噬的介质BNIP3、DRAM1和FUNDC1在子痫前期进展中的作用以及线粒体自噬途径在低出生体重病理生理中的作用。最近的研究表明，线粒体功能障碍和活性氧的积累与子痫前期和低出生体重有关。然而，由于该领域研究不足，结果存在争议。因此，与这些病理状况相关的线粒体自噬相关途径仍有待阐明。线粒体自噬相关途径是有望揭示子痫前期和低出生体重背后病理生理的研究靶点之一。
