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

Abstract

Purpose: Hypoxia alters mitochondria function and our aim was to measure mitochondrial fusion protein mitofusin-2 (Mfn2) in patients with preeclampsia.Materials and methods: 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.Results: 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, p < .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.Conclusion: 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.What do the results of this study add? 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.