Intrauterine growth restriction, human placental development and trophoblast cell death

摘要: Intrauterine growth restriction (IUGR) is a failure to achieve the potential of fetus that promised by genetic constitution and environmental influences endogenous pregnancy. Optimal placental development ability placenta compensate for stimulus-induced injury are central in promotion normal fetal growth. In this review, we will overview with focus on how villous structure relates function. We also describe differentiation turnover trophoblast while highlighting selected features microscopic injury. Histopathological studies IUGR indicate abnormalities maternal spiral arterioles, dysregulated vasculogenesis, abundant fibrin deposition characteristic injuries associated condition. identify insults, including oxidative stress complement activation, key pathways regulate apoptosis trophoblast, increased p53 activity, altered translation AKT mTOR proteins, response endoplasmic reticulum. surmise dysregulation at subcellular level loss functional mass via cell death contributors suboptimal performance yields IUGR. predict better understanding dysfunction lead targeted therapeutic options important clinical