The placenta is a highly vascularized and complex foetal organ that performs various tasks, crucial to a healthy pregnancy. Its dysfunction leads to complications such as stillbirth, preeclampsia, and intrauterine growth restriction. The specific cause of placental dysfunction remains unknown. Recently, the role of mitochondrial function and mitochondrial adaptations in the context of angiogenesis and placental dysfunction is getting more attention. The required energy for placental remodelling, nutrient transport, hormone synthesis, and the reactive oxygen species leads to oxidative stress, stemming from mitochondria. Mitochondria adapt to environmental changes and have been shown to adjust their oxygen and nutrient use to best support placental angiogenesis and foetal development. Angiogenesis is the process by which blood vessels form and is essential for the delivery of nutrients to the body. This process is regulated by different factors, pro-angiogenic factors and anti-angiogenic factors, such as sFlt-1. Increased circulating sFlt-1 levels have been linked to different preeclamptic phenotypes. One of many effects of increased sFlt-1 levels, is the dysregulation of mitochondrial function. This review covers mitochondrial adaptations during placentation, the importance of the anti-angiogenic factor sFlt-1in placental dysfunction and its role in the dysregulation of mitochondrial function.

中文翻译：

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胎盘线粒体功能作为血管生成和胎盘功能障碍的驱动因素


胎盘是一个高度血管化且复杂的胎儿器官，执行各种任务，对健康妊娠至关重要。它的功能障碍会导致死产、先兆子痫和宫内生长受限等并发症。胎盘功能障碍的具体原因尚不清楚。最近，线粒体功能和线粒体适应在血管生成和胎盘功能障碍中的作用越来越受到关注。胎盘重塑、营养物质运输、激素合成和活性氧所需的能量会导致来自线粒体的氧化应激。线粒体适应环境变化，并已被证明可以调整其氧气和营养物质的使用，以最好地支持胎盘血管生成和胎儿发育。血管生成是血管形成的过程，对于向身体输送营养物质至关重要。这一过程受到不同因素的调节，促血管生成因子和抗血管生成因子，例如sFlt-1。循环 sFlt-1 水平升高与不同的先兆子痫表型有关。 sFlt-1 水平升高的众多影响之一是线粒体功能失调。这篇综述涵盖了胎盘形成期间的线粒体适应、抗血管生成因子 sFlt-1 在胎盘功能障碍中的重要性及其在线粒体功能失调中的作用。