The origin of pre-eclampsia is associated with abnormal trophoblastic invasion, uteroplacental thrombophilia, and placental ischemic syndrome. Therefore, placental tissue is a source of pro-inflammatory cytokines, and a trigger for endothelial malfunction, oxidative stress, and systemic vasoconstriction. The maternal inflammatory response could be induced by necrotic or apoptotic changes in trophoblastic cells, HLA-incompatibility, and fetal DNA. The role of neuro-inflammation in the pathogenic scenario of pre-eclampsia is in the process of legitimization. The disturbed maternal hemodynamics is also associated with abnormally elevated intra-abdominal pressure. Pre-eclampsia increases the level of perinatal morbidity and mortality. The hypothesis of fetal programming explains its negative long-term consequences. The monitoring of fetal growth and neurodevelopment in pre-eclampsia is a prospect for a better understanding of perinatal pathology. The investigation of heart rate variability is a convenient tool for the detection of fetal neurological maturation. The disturbed maternal and fetal heart rate variability captures the effect of pre-eclampsia. Thus, maternal and fetal neuro-inflammation could be a part of the pathogenic pathways of pre-eclampsia.
Inflammation is involved in the pathogenic scenario of great obstetric syndromes, with this collection presenting novel findings in the field of pre-eclampsia. Pre-eclampsia is known to have short- and long-term consequences. The role of maternal inflammatory response in disturbed fetal neurological development and maturation is emphasized. Maternal neuro-inflammation is hypothesized as a possible trigger for pre-eclampsia. The monitoring of maternal and fetal heart rate variability is an instrument for the prediction and early detection of fetal compromise and delayed development. The possible strategy for the prevention of poor neurological outcomes and cardiovascular disease during adulthood is based on the antenatal period. The theoretical aspects of the march towards an improved fetal and newborn condition in pre-eclampsia are shown.
This Research Topic welcomes original research, review, and mini-review submissions on, but not limited to, the following aspects of innovations within the field:.
• The role of the placenta in immune regulation in pre-eclampsia.
• The issues of HLA-incompatibility in the pathogenic scenario of great obstetric syndromes.
• The systemic inflammatory response and neuroinflammation in the development of pre-eclampsia.
• Autoimmune disorders and antiphospholipid syndrome, and thrombophilia and inflammation in pre-eclampsia.
• The repercussions of maternal inflammation on fetal health, and further concerns on fetal programming.
• The maternal and perinatal outcomes of systemic inflammatory response syndrome.
• Vagal control of inflammation and maternal-fetal autonomic interaction in pre-eclampsia.
The origin of pre-eclampsia is associated with abnormal trophoblastic invasion, uteroplacental thrombophilia, and placental ischemic syndrome. Therefore, placental tissue is a source of pro-inflammatory cytokines, and a trigger for endothelial malfunction, oxidative stress, and systemic vasoconstriction. The maternal inflammatory response could be induced by necrotic or apoptotic changes in trophoblastic cells, HLA-incompatibility, and fetal DNA. The role of neuro-inflammation in the pathogenic scenario of pre-eclampsia is in the process of legitimization. The disturbed maternal hemodynamics is also associated with abnormally elevated intra-abdominal pressure. Pre-eclampsia increases the level of perinatal morbidity and mortality. The hypothesis of fetal programming explains its negative long-term consequences. The monitoring of fetal growth and neurodevelopment in pre-eclampsia is a prospect for a better understanding of perinatal pathology. The investigation of heart rate variability is a convenient tool for the detection of fetal neurological maturation. The disturbed maternal and fetal heart rate variability captures the effect of pre-eclampsia. Thus, maternal and fetal neuro-inflammation could be a part of the pathogenic pathways of pre-eclampsia.
Inflammation is involved in the pathogenic scenario of great obstetric syndromes, with this collection presenting novel findings in the field of pre-eclampsia. Pre-eclampsia is known to have short- and long-term consequences. The role of maternal inflammatory response in disturbed fetal neurological development and maturation is emphasized. Maternal neuro-inflammation is hypothesized as a possible trigger for pre-eclampsia. The monitoring of maternal and fetal heart rate variability is an instrument for the prediction and early detection of fetal compromise and delayed development. The possible strategy for the prevention of poor neurological outcomes and cardiovascular disease during adulthood is based on the antenatal period. The theoretical aspects of the march towards an improved fetal and newborn condition in pre-eclampsia are shown.
This Research Topic welcomes original research, review, and mini-review submissions on, but not limited to, the following aspects of innovations within the field:.
• The role of the placenta in immune regulation in pre-eclampsia.
• The issues of HLA-incompatibility in the pathogenic scenario of great obstetric syndromes.
• The systemic inflammatory response and neuroinflammation in the development of pre-eclampsia.
• Autoimmune disorders and antiphospholipid syndrome, and thrombophilia and inflammation in pre-eclampsia.
• The repercussions of maternal inflammation on fetal health, and further concerns on fetal programming.
• The maternal and perinatal outcomes of systemic inflammatory response syndrome.
• Vagal control of inflammation and maternal-fetal autonomic interaction in pre-eclampsia.