Abstract
Intrauterine growth restriction (IUGR) is an obstetric complication characterised by placental insufficiency and secondary cardiovascular remodelling that can lead to cardiomyopathy in adulthood. Despite its aetiology and potential therapeutics are poorly understood, bioenergetic deficits have been demonstrated in adverse foetal and cardiac development. We aimed to evaluate the role of mitochondria in human pregnancies with IUGR. In a single‐site, cross‐sectional and observational study, we included placenta and maternal peripheral and neonatal cord blood mononuclear cells (PBMC and CBMC) from 14 IUGR and 22 control pregnancies. The following mitochondrial measurements were assessed: enzymatic activities of mitochondrial respiratory chain (MRC) complexes I, II, IV, I + III and II + III, oxygen consumption (cell and complex I‐stimulated respiration), mitochondrial content (citrate synthase [CS] activity and mitochondrial DNA copy number), total ATP levels and lipid peroxidation. Sirtuin3 expression was evaluated as a potential regulator of bioenergetic imbalance. Intrauterine growth restriction placental tissue showed a significant decrease of MRC CI enzymatic activity (P < 0.05) and CI‐stimulated oxygen consumption (P < 0.05) accompanied by a significant increase of Sirtuin3/β‐actin protein levels (P < 0.05). Maternal PBMC and neonatal CBMC from IUGR patients presented a not significant decrease in oxygen consumption (cell and CI‐stimulated respiration) and MRC enzymatic activities (CII and CIV). Moreover, CS activity was significantly reduced in IUGR new‐borns (P < 0.05). Total ATP levels and lipid peroxidation were preserved in all the studied tissues. Altered mitochondrial function of IUGR is especially present at placental and neonatal level, conveying potential targets to modulate obstetric outcome through dietary interventions aimed to regulate Sirtuin3 function.
Highlights
Intrauterine growth restriction (IUGR) is a common pregnancy com‐ plication that arises when the foetus does not achieve its growth potential and affects 5%‐10% of all pregnancies.[1,2] Recent evidence demonstrated that IUGR is associated with foetal cardiovascular re‐ modelling (CVR)[5,6] which may eventually result in a cardiovascular risk in adulthood.[7,8]the aetiopathology that underlies IUGR is still a matter of doubt
Previous experimental studies pointed out that mitochondrial deficits play a relevant role in IUGR and associated CVR.[33,34]
Few and contrasting studies were found in the literature investigating mito‐ chondrial alterations in human pregnancies, pointing out the need for a wider study of mitochondrial involvement in patients with this obstetric complication
Summary
Intrauterine growth restriction (IUGR) is a common pregnancy com‐ plication that arises when the foetus does not achieve its growth potential and affects 5%‐10% of all pregnancies.[1,2] Recent evidence demonstrated that IUGR is associated with foetal cardiovascular re‐ modelling (CVR)[5,6] which may eventually result in a cardiovascular risk in adulthood.[7,8]the aetiopathology that underlies IUGR is still a matter of doubt. Intrauterine growth restriction (IUGR) is a common pregnancy com‐ plication that arises when the foetus does not achieve its growth potential and affects 5%‐10% of all pregnancies.[1,2] Recent evidence demonstrated that IUGR is associated with foetal cardiovascular re‐ modelling (CVR)[5,6] which may eventually result in a cardiovascular risk in adulthood.[7,8]. IUGR is associated with placental insuffi‐ ciency.[11,12] The placenta is the organ enabling nutrient and oxygen supply to the foetus.[14,15] it plays a pivotal role for the adequate foetal development, since it requires high energy produc‐ tion for metabolic processes and cell growth.[16,17]
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