Preeclampsia is a pregnancy-specific syndrome with multisystem involvement which leads to foetal, neonatal, and maternal morbidity and mortality. This syndrome characterizes 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 differential involvement of mitochondrial dysfunction 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 with altered mitochondria structure and function resulting in ROS overproduction, oxidative stress, and cell damage and death. Mitochondria dysfunction may result from different alterations in eoPE where an 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. However, 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 expression of essential proteins involved in the electron transport chain is reduced, leading to lower oxidative phosphorylation and mitochondrial respiration in the placenta in preeclampsia. Interventional studies in patients with preeclampsia using the coenzyme Q10, a key molecule in the electron transport chain, suggest that agents increasing the antioxidant capacity of the placenta may be protective of developing preeclampsia. In this review, the mitochondrial dysfunction in both eoPE and loPE is summarized. Therapeutical approaches are discussed in the context of contributing to the understanding of mitochondrial dysfunction in eoPE and loPE.
Oxidative stress and mitochondrial dysfunction in early-onset and late-onset preeclampsia