Chronic hypoxaemia as a molecular regulator of fetal lung development: implications for risk of respiratory complications at birth.
Exposure to altered intrauterine conditions during pregnancy influences both fetal growth and organ development. Chronic fetal hypoxaemia is a common pregnancy complication associated with intrauterine growth restriction (IUGR) that may influence the risk of infants experiencing respiratory complications at birth. There are a variety of signalling pathways that contribute to normal fetal lung development at the molecular level. The specific molecular effects of chronic hypoxaemia associated with IUGR on lung development are likely to be dependent on the specific aetiology (maternal, placental and/or fetal factors) that can alter hormone concentrations, oxygen and nutrient transport to the fetus. This review discusses molecular pathways that may contribute to altered fetal lung maturation following exposure to chronic hypoxaemia. Importantly, these studies highlight that the heterogeneity in respiratory outcomes at birth in this obstetric subpopulation are likely determined by the timing, severity and duration of chronic hypoxaemia encountered by the fetus during pregnancy.
Early Origins of Adult Health Research Group; Molecular and Evolutionary Physiology of the Lung Laboratory, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia. Electronic address: erin.mcgillick@mymail.unisa.edu.au.
Erin V
EV
McGillick
Molecular and Evolutionary Physiology of the Lung Laboratory, School of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, Australia. Electronic address: Sandra.Orgeig@unisa.edu.au.
Sandra
S
Orgeig
Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridgeshire, United Kingdom. Electronic address: dag26@cam.ac.uk.
Dino A
DA
Giussani
Early Origins of Adult Health Research Group. Electronic address: Janna.Morrison@unisa.edu.au.
Janna L
JL
Morrison
D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D005260:Female; D005317:Fetal Growth Retardation / Q000453:epidemiology* / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D000860:Hypoxia / Q000453:epidemiology* / Q000235:genetics / Q000378:metabolism; D007231:Infant, Newborn; D008168:Lung / Q000196:embryology*; D018384:Oxidative Stress; D011247:Pregnancy; D011248:Pregnancy Complications / Q000453:epidemiology* / Q000235:genetics / Q000378:metabolism; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology* / Q000235:genetics / Q000378:metabolism; D011663:Pulmonary Surfactants / Q000378:metabolism; D012127:Respiratory Distress Syndrome, Newborn / Q000453:epidemiology* / Q000235:genetics / Q000378:metabolism; D012756:Sheep; D015398:Signal Transduction
D011663:Pulmonary Surfactants
Fetal lung; chronic hypoxaemia; intrauterine growth restriction; oxidative stress; pulmonary surfactant; respiratory distress syndrome