Preeclampsia is a pregnancy-specific syndrome with multisystem involvement which leads to foetal, neonatal, and maternal morbidity and mortality. This syndrome is characterized by the onset of clinical signs and symptoms and delivery before (early-onset preeclampsia, eoPE), or after (late-onset preeclampsia, loPE), the 34 weeks of gestation. Preeclampsia is a mitochondrial disorder where its differential involvement in eoPE and loPE is unclear. Mitochondria regulate cell metabolism and are a significant source of reactive oxygen species (ROS). The syncytiotrophoblast in eoPE and loPE show altered mitochondrial structure and function resulting in ROS overproduction, oxidative stress, and cell damage and death. Mitochondrial dysfunction in eoPE may result from altered expression of several molecules, including dynamin-related protein 1 and mitofusins, compared with loPE where these factors are either reduced or unaltered. Equally, mitochondrial fusion/fission dynamics seem differentially modulated in eoPE and loPE. It is unclear whether the electron transport chain and oxidative phosphorylation are differentially altered in these two subgroups of preeclampsia. However, the activity of complex IV (cytochrome c oxidase) and the expression of essential proteins involved in the electron transport chain are reduced, leading to lower oxidative phosphorylation and mitochondrial respiration in the preeclamptic placenta. Interventional studies in patients with preeclampsia using the coenzyme Q₁₀, a key molecule in the electron transport chain, suggest that agents that increase the antioxidative capacity of the placenta may be protective against preeclampsia development. In this review, the mitochondrial dysfunction in both eoPE and loPE is summarized. Therapeutic approaches are discussed in the context of contributing to the understanding of mitochondrial dysfunction in eoPE and loPE.

先兆子痫是一种特定于妊娠的综合症，涉及多系统，导致胎儿，新生儿和产妇的发病和死亡。该综合征的特征是在妊娠34周之前（早发先兆子痫，eoPE）或之后（迟发先兆子痫，loPE）开始临床体征和症状并分娩。子痫前期是线粒体疾病，其在eoPE和loPE中的差异参与尚不清楚。线粒体调节细胞代谢，并且是活性氧（ROS）的重要来源。eoPE和loPE中的合体滋养层细胞显示出改变的线粒体结构和功能，导致ROS过度产生，氧化应激以及细胞损伤和死亡。eoPE的线粒体功能障碍可能是由于几种分子表达的改变，与loPE相比，包括与动力相关的蛋白1和线粒体融合素，其中这些因素被降低或未改变。同样，线粒体融合/裂变动力学在eoPE和loPE中似乎有不同的调节。目前尚不清楚先兆子痫的这两个亚组中的电子传输链和氧化磷酸化是否差异性改变。然而，复合物IV（细胞色素c氧化酶）和电子传输链中涉及的必需蛋白的表达降低，导致先兆子痫前胎盘中的氧化磷酸化作用和线粒体呼吸作用降低。使用电子传输链中的关键酶辅酶Q ₁₀对子痫前期患者进行的干预研究表明，增加胎盘抗氧化能力的药物可以预防子痫前期的发展。在这篇综述中，总结了eoPE和loPE中的线粒体功能障碍。在有助于了解eoPE和loPE中线粒体功能障碍的背景下讨论了治疗方法。