Prenatal hypoxia and cardiac programming.
Epidemiologic studies have shown a clear association of adverse intrauterine environment and an increased risk of hypertension and coronary heart disease in the adult. Many studies have been focused on the effects of maternal undernutrition and fetal glucocorticoid exposure on fetal programming and later adult disease. Although it is relatively less clear, there is evidence that fetal exposure to hypoxia, alcohol, tobacco smoking, and cocaine may also cause in utero programming leading to an increased risk of adult disease. Chronic hypoxia during the course of pregnancy is thought to result in fetal intrauterine growth retardation. Among other effects, chronic hypoxia suppresses fetal cardiac function, alters cardiac gene expression, increases myocyte apoptosis, and results in a premature exit of the cell cycle of cardiomyocytes and myocyte hypertrophy. This review discusses recent evidence of an association of prenatal hypoxic exposure with an increased vulnerability of adult heart disease, and the possible mechanisms involved.
Zhang
Lubo
L
Center for Perinatal Biology, Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, California 92350, USA. lzhang@som.llu.edu
D000328:Adult; D000428:Alcohol Drinking / Q000009:adverse effects; D019970:Cocaine-Related Disorders / Q000150:complications; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005311:Fetal Hypoxia / Q000150:complications*; D018507:Gene Expression Regulation, Developmental; D006321:Heart / Q000196:embryology*; D006331:Heart Diseases / Q000209:etiology*; D006801:Humans; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects