Hypertensive disorders of pregnancy including preeclampsia are disturbances that may often result in fetal growth restriction. However, underlying mechanisms linking nitric oxide and matrix metalloproteinases are still unclear. The development of these severe conditions can be influenced by lifestyle, obesity, inflammation, as well as genetic and environmental factors.
In search for understanding the causes, reduced uteroplacental perfusion pressure along with placental ischemia have recently been raised as key pathophysiological triggers. Ischemic placenta may release active factors within the systemic circulation of the mother which commonly leads to angiogenic imbalance, proinflammatory state, and oxidative stress. Under this condition, maternal endothelial cells become more susceptible to the endothelial dysfunction, which compromise, in general, the function of cerebral, renal, and hepatic arteries. Potential targets have received attention, particularly, nitric oxide and matrix metalloproteinases. These bioactive factors are possibly key players in maintaining adequate vascular remodeling at the maternal-fetal interface, thus, future therapies may depend on clarifying the underlying mechanisms that underpin endothelial dysfunction. Therefore, the aim of this Research Topic is to share the latest findings related to these bioactive factors in Hypertensive disorders of pregnancy and preeclampsia.
Hypertensive disorders of pregnancy including preeclampsia are disturbances that may often result in fetal growth restriction. However, underlying mechanisms linking nitric oxide and matrix metalloproteinases are still unclear. The development of these severe conditions can be influenced by lifestyle, obesity, inflammation, as well as genetic and environmental factors.
In search for understanding the causes, reduced uteroplacental perfusion pressure along with placental ischemia have recently been raised as key pathophysiological triggers. Ischemic placenta may release active factors within the systemic circulation of the mother which commonly leads to angiogenic imbalance, proinflammatory state, and oxidative stress. Under this condition, maternal endothelial cells become more susceptible to the endothelial dysfunction, which compromise, in general, the function of cerebral, renal, and hepatic arteries. Potential targets have received attention, particularly, nitric oxide and matrix metalloproteinases. These bioactive factors are possibly key players in maintaining adequate vascular remodeling at the maternal-fetal interface, thus, future therapies may depend on clarifying the underlying mechanisms that underpin endothelial dysfunction. Therefore, the aim of this Research Topic is to share the latest findings related to these bioactive factors in Hypertensive disorders of pregnancy and preeclampsia.
