Abstract
Maternal diabetes is a prevalent pathology that increases the risk of cardiovascular diseases in the offspring, the heart being one of the main target organs affected from the fetal stage until the adult life. Metabolic, pro-oxidant, and proinflammatory alterations in the fetal heart constitute the first steps in the adverse fetal programming of cardiovascular disease in the context of maternal diabetes. This review discusses both human and experimental studies addressing putative mechanisms involved in this fetal programming of heart damage in maternal diabetes. These include cardiac epigenetic changes, alterations in cardiac carbohydrate and lipid metabolism, damaging effects caused by a pro-oxidant and proinflammatory environment, alterations in the cardiac extracellular matrix remodeling, and specific signaling pathways. Putative actions to prevent cardiovascular impairments in the offspring of mothers with diabetes are also discussed.
Highlights
Cardiovascular diseases are increasing at alarming rates in both developed and developing countries (Balakumar et al, 2016; Bhatnagar et al, 2016)
This study showed that several of the top 10 genes ranked by statistical significance, such as Natriuretic Peptide Receptor 1 (NPR1; related to blood pressure homeostasis), panthothenate kinase (PANK1; a critical enzyme in the synthesis of coenzyme A), SCAN domain-containing protein 1 (SCAND1; which encodes a cofactor that interacts with transcription factor regulators of genes involved in lipid metabolism), and GJA4 were associated with cardiovascular risk (West et al, 2013)
We have evaluated a maternal treatment with the mitochondrial antioxidant idebenone in a model of mild diabetes during pregnancy to address the role of oxidative stress and mitochondrial dysfunction in the programming of cardiac alterations and observed that this treatment prevents the increase in markers of oxidative damage in the heart of offspring from diabetic rats at a prepubertal stage (Higa et al, 2017)
Summary
Reviewed by: Julienne Rutherford, University of Illinois at Chicago, United States Helen Jones, Cincinnati Children's Hospital Medical Center, United States. Pro-oxidant, and proinflammatory alterations in the fetal heart constitute the first steps in the adverse fetal programming of cardiovascular disease in the context of maternal diabetes. This review discusses both human and experimental studies addressing putative mechanisms involved in this fetal programming of heart damage in maternal diabetes. These include cardiac epigenetic changes, alterations in cardiac carbohydrate and lipid metabolism, damaging effects caused by a pro-oxidant and proinflammatory environment, alterations in the cardiac extracellular matrix remodeling, and specific signaling pathways.
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