Innate immunity and blood coagulation systems are the first line of defense against mechanical injury and infection. Immune cells can initiate the coagulation cascade and coagulation regulators can recruit immune cells to the site of injury. A successful mammalian pregnancy requires precise modulation of both systems to overcome the hemostatic challenges of hemochorial placentation and to maintain central and peripheral tolerance towards the semiallogeneic fetus. Despite major discoveries in immunology and coagulation research, there remain fundamental gaps in knowledge on how coagulation and immune regulation work and interact in placentation and pregnancy. Human reproduction involves hemochorial placentation where maternal blood physiologically leaves blood vessels and directly bathes specialized extraembryonic cells, called trophoblast cells. While this arrangement ensures intimate contact between the mother and the fetus, it also poses significant risks of hemorrhage, organ-specific thrombosis and thrombo-inflammation. Non-vascular cells, such as extraembryonic trophoblasts, participate in maintaining placental hemostasis. New roles of coagulation regulators in trophoblast cell invasion have begun to emerge. Animal models further highlight a critical role of coagulation factors in placentation and healthy maternal and fetal outcomes. In human pregnancy, decidual thrombosis is frequently seen in association with fetal growth restriction, placental abruption, preeclampsia, and preterm birth. Preeclampsia, in particular the Hemolysis, Elevated Liver enzymes, Low Platelet (HELLP) syndrome, involves platelet activation. The function of coagulation regulators in pregnancy complications appears to extend beyond the control of hemostasis. Coagulation-inflammation crosstalk and the downstream mechanisms that lead to pregnancy complications are beginning to be identified.
The goal of this collection is to put together evidence-based data evaluating the role of aberrant coagulation, inflammation, and thromboinflammation in pregnancy complications. We expect the collection to be interdisciplinary, drawing upon work in basic science studies on cell models, animal models as well as clinical, epidemiological and population-based evaluation of human pregnancy and its complications.
The section welcomes the following article types: Original Research, Review, Mini-Review, Methods, Perspective, Opinion, Editorial, General Commentary, Data Report, Hypothesis and Theory.
Specific topics of interest include but are not limited to:
• Hemostatic changes of pregnancy
• Placental hemostasis
• Animal models of aberrant blood coagulation and pregnancy complications
• Inherited thrombophilia and pregnancy complications
• Antiphospholipid syndrome and pregnancy complications
• Coagulation and platelet activation in pregnancy complications
• Coagulation-inflammation crosstalk in pregnancy complications
• New clinical insights into detecting and treating thromboinflammation in pregnancy complications.
Innate immunity and blood coagulation systems are the first line of defense against mechanical injury and infection. Immune cells can initiate the coagulation cascade and coagulation regulators can recruit immune cells to the site of injury. A successful mammalian pregnancy requires precise modulation of both systems to overcome the hemostatic challenges of hemochorial placentation and to maintain central and peripheral tolerance towards the semiallogeneic fetus. Despite major discoveries in immunology and coagulation research, there remain fundamental gaps in knowledge on how coagulation and immune regulation work and interact in placentation and pregnancy. Human reproduction involves hemochorial placentation where maternal blood physiologically leaves blood vessels and directly bathes specialized extraembryonic cells, called trophoblast cells. While this arrangement ensures intimate contact between the mother and the fetus, it also poses significant risks of hemorrhage, organ-specific thrombosis and thrombo-inflammation. Non-vascular cells, such as extraembryonic trophoblasts, participate in maintaining placental hemostasis. New roles of coagulation regulators in trophoblast cell invasion have begun to emerge. Animal models further highlight a critical role of coagulation factors in placentation and healthy maternal and fetal outcomes. In human pregnancy, decidual thrombosis is frequently seen in association with fetal growth restriction, placental abruption, preeclampsia, and preterm birth. Preeclampsia, in particular the Hemolysis, Elevated Liver enzymes, Low Platelet (HELLP) syndrome, involves platelet activation. The function of coagulation regulators in pregnancy complications appears to extend beyond the control of hemostasis. Coagulation-inflammation crosstalk and the downstream mechanisms that lead to pregnancy complications are beginning to be identified.
The goal of this collection is to put together evidence-based data evaluating the role of aberrant coagulation, inflammation, and thromboinflammation in pregnancy complications. We expect the collection to be interdisciplinary, drawing upon work in basic science studies on cell models, animal models as well as clinical, epidemiological and population-based evaluation of human pregnancy and its complications.
The section welcomes the following article types: Original Research, Review, Mini-Review, Methods, Perspective, Opinion, Editorial, General Commentary, Data Report, Hypothesis and Theory.
Specific topics of interest include but are not limited to:
• Hemostatic changes of pregnancy
• Placental hemostasis
• Animal models of aberrant blood coagulation and pregnancy complications
• Inherited thrombophilia and pregnancy complications
• Antiphospholipid syndrome and pregnancy complications
• Coagulation and platelet activation in pregnancy complications
• Coagulation-inflammation crosstalk in pregnancy complications
• New clinical insights into detecting and treating thromboinflammation in pregnancy complications.
