Maternal serum mitofusin-2 levels in patients with preeclampsia: the possible role of mitochondrial dysfunction in preeclampsia

Abstract

<b>Purpose:</b> Hypoxia alters mitochondria function and our aim was to measure mitochondrial fusion protein mitofusin-2 (Mfn2) in patients with preeclampsia.<b>Materials and methods:</b> This cross-sectional study was conducted including 82 pregnant women, 27 with normal pregnancy and 55 with preeclampsia (27 with early-onset preeclampsia and 28 with late-onset preeclampsia). Maternal serum levels of Mfn2 were measured by using enzyme-linked immunosorbent assay kits.<b>Results:</b> The mean serum mitofusin-2 levels were higher in women with preeclampsia than in the control group (68.02 ± 8.7 pg/mL vs. 99.72 ± 37.27 pg/mL, <i>p</i> < .0001). The mean serum mitofusin-2 level was found to be the highest in the early-onset preeclampsia (EOPE) group (EOPE: 101.6 ± 38.5 pg/mL). Maternal serum mitofusin-2 levels correlated with both systolic and diastolic blood pressures as well as uterine artery pulsatility index. The optimal cutoff value of Mfn2 for determining preeclampsia was 75.3 pg/mL.<b>Conclusion:</b> Mfn2 has regulatory roles in stress response. Maternal serum Mfn2 is higher in patients with preeclampsia suggesting that Mfn2 increases in the maternal system as a stress response against hypoxia and endothelial dysfunction.<b>What do the results of this study add?</b> Hypoxia causes mitochondrial dysfunction that has been linked to the etiology of many diseases including preeclampsia. Mitofusin-2 is a mitochondrial fusion protein, and the levels can be altered in preeclampsia. For the first time, we showed that maternal levels of mitofusin-2 are higher in patients with preeclampsia. Further, we reported the correlation of mitofusin-2 with blood pressures and uterine artery pulsatility index. These findings will open up other avenues for researchers to investigate other mitochondrial molecules while under stress.