Coenzyme Q10 prevents accelerated cardiac aging in a rat model of poor maternal nutrition and accelerated postnatal growth
Year: 2013
Type: article
Abstract: Studies in human and animals have demonstrated that nutritionally induced low birth-weight followed by rapid postnatal growth increases the risk of metabolic syndrome and cardiovascular disease. Although the mechanisms underlying such nutritional programming are not clearly defined, increased oxidative-stress leading to accelerated cellular aging has been proposed to play an important role. Using an established rodent model of low birth-weight and catch-up growth, we show here that post-weaning dietary supplementation with coenzyme Q10, a key component of the electron transport chain and a potent antioxidant rescued many of the detrimental effects of nutritional programming on cardiac aging. This included a reduction in nitrosative and oxidative-stress, telomere shortening, DNA damage, cellular senescence and apoptosis. These findings demonstrate the potential for postnatal antioxidant intervention to reverse deleterious phenotypes of developmental programming and therefore provide insight into a potential translatable therapy to prevent cardiovascular disease in at risk humans.
Source: Molecular Metabolism
Language: English
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $4,270
Awards: Mitochondrial targeted antioxidant therapy against programming of cardiovascular disease by developmental hypoxia, Hypoxia and Reactive Oxygen Species in Fetal Cardiovascular Function, A role for a programmed mitochondrial CoQ deficit in developmental programming of cardiovascular disease, Molecular mechanisms by which poor early growth links coronary artery disease, insulin resistance and type 2 diabetes
OpenAlex ID: W2101176463
