Fetal Programming of cardiovascular diseases in maternal diabetes.

ROMINA HIGA, MARÍA LAURA LEONARDI, EVANGELINA CAPOBIANCO, ALICIA JAWERBAUM

Congreso; Reunión anual de Sociedades Biocientíficas (SAIC 2021); 2021

Cardiovascular diseases are increasing at alarming rates in both developed and developing countries. Al- though lifestyle choices and genetic predisposition are main contributors to cardiometabolic diseases, growing evidence indicates that in utero exposure to adverse en- vironmental conditions leads the developing offspring to have numerous risk factors, which may have an impact later in life.Maternal diabetes is a prevalent pathology that increases the risk of cardiovascular diseases in the offspring. The heart is one of the main target organs affected by this metabolic disease from the embryonic stage and until the adult life. Putative mechanism involved in intrauterine programming of heart damage evidenced in experimen- tal models of maternal diabetes will be presented. The focus will be on altered pathways that regulates cardiac cellular metabolism, the damaging effects of the proo- xidant and proinflammatory environment and alterations on the cardiac extracellular matrix remodeling. The role of three main players of these pathways will be discussed: mechanistic target of rapamycin, a cellular sensor for energy metabolism and nutrient availability that controls cellular growth and metabolism, peroxisome proliferator activated receptors, nuclear receptors highly involved in heart metabolic processes and lipid metabolism and the transcription factor forkhead box protein O1 which partic- ipates in myocardial metabolic stress adaptation, oxida- tive stress, endothelial dysfunction and other processes related to inflammation and apoptosis.All these pathways are interconnected evidencing the complexity of this process but also bringing opportunities to facilitate intervention to provide protective effects to prevent the programming of cardiovascular diseases in the offspring of diabetic rats