Researchers at Cambridge University discovered that a specialized antioxidant called MitoQ can prevent heart disease at its very onset.
The study is published in Science Advances in a paper titled, “Translatable mitochondria-targeted protection against programmed cardiovascular dysfunction,” and led by Dino Giussani, PhD, professor at the University of Cambridge’s department of physiology, development, and neuroscience.
“Using sheep and chickens, two species with similar cardiovascular developmental milestones to humans, we combined in vivo experiments with in vitro studies at organ, cellular, mitochondrial, and molecular levels,” noted the researchers. “We tested mitochondria-targeted antioxidant intervention with MitoQ against cardiovascular dysfunction programmed by developmental hypoxia, a common complication in human pregnancy. Experiments in sheep determined in vivo fetal and adult cardiovascular function through surgical techniques not possible in humans, while those in chicken embryos isolated effects independent of maternal or placental influences.”
Genetics, lifestyle risk factors such as smoking, diabetes, and obesity, play a role in determining heart disease risk in adults. There is strong evidence that points to the environment experienced during sensitive periods of fetal development directly influencing long-term cardiovascular issues. Chronic fetal hypoxia, which occurs when the fetus is deprived of an adequate supply of oxygen, is one of the most common complications in human pregnancy. In a process called “oxidative stress,” low oxygen to the developing fetus can cause damage to its heart and blood vessels.
“Many people may be predisposed to heart disease as adults because of the low level of oxygen they received in the womb. By providing a specific mitochondria-targeted antioxidant supplement to mothers whose pregnancy is complicated by fetal hypoxia, we can potentially prevent this,” explained Giussani.
Mitochondria are a major site of reactive oxygen species production, which determined the researchers’ therapeutic strategy. However, conventional antioxidants are ineffective because they cannot readily penetrate the mitochondria.
The researchers used MitoQ, developed by Mike Murphy, PhD, program leader, and his colleagues at the University of Cambridge’s MRC-Mitochondrial Biology Unit. MitoQ selectively accumulates within mitochondria, where it works to reduce oxidative stress.
The researchers gave MitoQ to pregnant sheep under low oxygen conditions. They found that the mitochondrial therapy protected against fetal growth restriction and high blood pressure in the offspring as adults. Using chicken embryos they also showed that MitoQ protects against mitochondria-derived oxidative stress.
“We show that hypoxia generates mitochondria-derived oxidative stress during cardiovascular development, programming endothelial dysfunction and hypertension in adult offspring. MitoQ treatment during hypoxic development protects against this cardiovascular risk via enhanced nitric oxide signaling, offering a plausible intervention strategy,” the researchers wrote.
“Our cardiovascular health is influenced by the lifestyle choices we make in adult life, but can also be traced back to the conditions we experienced when developing inside the womb,” noted James Leiper, PhD, professor and associate medical director at the British Heart Foundation.
“This study reveals a plausible way to reduce the future risk of high blood pressure and consequent heart disease in babies from complicated pregnancies,” Leiper added.
Leiper stresses further research is needed to translate their findings from animals to humans to identify the most effective time to give the MitoQ supplement to babies at risk.
“If we want to reduce the prevalence of cardiovascular disease, we need to think of prevention rather than a cure. Applying this concept to pregnancy complications, we can bring preventative medicine all the way back into the womb—it’s treatment before birth. It completely changes our way of thinking about heart disease,” concluded Giussani.