Fig. 6. Summary illustration: Protective effects of MitoQ treatment in hypoxic development.

The mitochondria-targeted antioxidant MitoQ protects the chronically hypoxic fetus from cardiovascular dysfunction and remodeling, which programs adult-onset peripheral vascular dysfunction and systemic hypertension. These protective effects of MitoQ in the compromised fetus occur without affecting the fetal brain–sparing hemodynamic response to acute hypoxia. Mechanisms underlying benefits of MitoQ on the offspring cardiovascular system include direct protection against mitochondria-derived oxidative stress and normalization of cardiac mitochondrial respiration in the hypoxic embryo, together with programmed increases in circulating NO bioavailability and in peripheral vascular sensitivity to it in the adult offspring. MitoQ treatment in sheep protects against fetal growth restriction in hypoxic pregnancy. In contrast, MitoQ treatment in hypoxic chicken embryos does not affect growth restriction. Therefore, protective effects of MitoQ on fetal growth in mammals may occur at the level of the placenta.