Effect of glucocorticoids on mechanisms of placental angiogenesis |
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| Affiliation: | 1. Irish Centre for Fetal and Neonatal Translation Research (INFANT), Cork University Maternity Hospital, University College Cork, Cork, Ireland;2. Department of Obstetrics and Gynaecology, Cork University Maternity Hospital, University College Cork, Cork, Ireland;3. Department of Anatomy and Neuroscience, University College Cork, Cork, Ireland;1. Mater Research Institute – The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia;2. School of Medical Science, Menzies Health Institute Queensland, Griffith University, Gold Coast, Australia;3. School of Biomedical Sciences and Centre for Child Health Research, The University of Queensland, Brisbane, Australia;4. Monash Biomedicine Discovery Institute, Monash University, Melbourne, Australia;5. Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Monash Medical Centre, Melbourne, Australia;6. Division of Allergy-Immunology, Department of Medicine, Northwestern University, Chicago, IL, USA;1. Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, China;2. Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China;3. Hubei Provincial Key Laboratory of Developmentally Originated Disease, Wuhan 430071, China |
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| Abstract: | The benefits of antenatal glucocorticoid (GC) treatment to promote human fetal lung maturation are well established. However, reports have emerged indicating that maternal exposure to high concentrations of circulating GCs alters placental and fetal development. Because many adult-onset metabolic and cardiovascular disorders have their origins in utero, the importance of prenatal conditions should be considered in detail. Therefore, this review aims to present an overview of the GC effect on placental and fetal development, specifically with regard to mechanisms of placental angiogenesis.We assumed that GC overexposure affects fetal development by altering placental angiogenesis. Disturbances in the development of the villous tree and pathological changes in the villous vascular system with insufficient uteroplacental blood flow have been linked to the pathogenesis of intrauterine growth retardation. Moreover, low birth weight is a serious risk factor known to correlate with an increased risk of adult-onset diseases. Although there have been many circumstances in which maternal GCs are elevated, we focused on exogenous synthetic GCs that are applied for therapeutic reasons. However, some questions about the use of steroids remain unanswered, which will require further studies that lead us to review alterations in placental angiogenesis under the perspective of GC overexposure. |
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| Keywords: | Glucocorticoids Placenta Angiogenesis Human Rat |
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