Recent Advances in Placental Pathophysiology
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (1 March 2023) | Viewed by 5757
Special Issue Editor
Special Issue Information
Dear Colleagues,
Every year, around 20 % of 140 million births worldwide are from pathological pregnancies. These obstetrical complications have lifelong consequences for the mother (death, metabolic disorders) and the foetus (death, intrauterine growth restriction (IUGR), prematurity, and metabolic disorders in adulthood). Many complications of pregnancy, including implantation failure, miscarriage, IUGR and preeclampsia, are related to placental or uterine placental interface dysfunctions. The placenta is directly involved in the initiation and outcome of gestation, foetal growth and development.
Despite the high incidence of obstetrical complications, little is known about the mechanisms involved in the development of this transitory organ that is essential to life.
The placenta is essential for implantation, enables an immune tolerance of the conceptus to avoid miscarriage, produces pregnancy hormones such as hCG at implantation to maintain pregnancy, participates in the remodelling of the uterine spiral arteries, is a biological barrier allowing the exchange of nutrients and gases between maternal and foetal blood, protects the foetus from toxics and pathogens, and might be involved in parturition.
Poor placentation is directly involved in many pregnancy-related diseases, such as preeclampsia, foetal growth restriction, and prematurity.
Preeclampsia is a major complication of pregnancy that affects 2% to 7% of pregnant women. It is characterized by hypertension and de novo proteinuria during the second half of pregnancy. The exact pathogenesis of preeclampsia is far from fully understood, but placental dysfunction is considered to play a central role. A three-stage pathophysiological model of preeclampsia has been described, which comprises an immunological conflict between mother and embryo, defective trophoblast invasion and faulty remodelling of the uterine vasculature. It also causes placental hypoperfusion, which alters villous trophoblasts and increases the release of pro-/anti-angiogenic factors into the maternal circulation, leading to an excessive maternal inflammatory response and endothelial dysfunction (stage 3).
Intrauterine growth restriction (IUGR) is frequently associated with preeclampsia. It is one of the main causes of perinatal morbidity and mortality and results in long-term metabolic complications (type 2 diabetes, metabolic syndrome).
Sub-topics:
- Interactions between trophoblasts and uterine immune cells;
- Trophoblastic cell differentiation, proliferation, invasion, fusion, apoptosis, necrosis and senescence;
- Remodelling of uterine spiral arteries;
- Genetic, Epigenetic (DOHAD: developmental origin of health and disease);
- Pollutants: endocrine disruptors, xenobiotics, drugs;
- Infectious diseases;
- Maternal microbiota.
Dr. Thierry Fournier
Guest Editor
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Keywords
- pregnancy
- preeclampsia
- prematurity
- FGR
- pollutants
- genetic
- epigenetic
- infections
