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Low birth weight has been widely shown to be correlated withdrastically increased risk of developing adult cardiovasculardiseases. Unfortunately, the cause of this association isrelatively unknown. This work explores the possible mechanisms thatunderlie this association, with focus on the insulin-like growthfactor (IGF) axis. IGFs are essential regulators of fetal growth.Their effects are modulated by the IGF binding proteins (IGFBPs).Circulating IGFBP-1 levels are elevated in growth-restricted humanfetuses, and fetal growth restriction increases the risk ofcardiovascular diseases in…mehr

Produktbeschreibung
Low birth weight has been widely shown to be correlated withdrastically increased risk of developing adult cardiovasculardiseases. Unfortunately, the cause of this association isrelatively unknown. This work explores the possible mechanisms thatunderlie this association, with focus on the insulin-like growthfactor (IGF) axis. IGFs are essential regulators of fetal growth.Their effects are modulated by the IGF binding proteins (IGFBPs).Circulating IGFBP-1 levels are elevated in growth-restricted humanfetuses, and fetal growth restriction increases the risk ofcardiovascular diseases in adulthood. This work reveals thattransgenic mice with elevated levels of circulating IGFBP-1 in lategestation are growth restricted, and have altered cardiacmorphology and function. This altered development likely leads tosignificant impairments in cardiac morphology and function inadulthood, therefore contributing to increased risk ofcardiovascular diseases.