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Prenatal hypoxia and cardiac programming

Journal

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jsgi.2004.09.004

Keywords

hypoxia; fetal programming; heart

Funding

  1. NHLBI NIH HHS [HL-57787, HL-67745] Funding Source: Medline
  2. NICHD NIH HHS [HD-31226] Funding Source: Medline
  3. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD031226] Funding Source: NIH RePORTER
  4. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL067745, R01HL057787] Funding Source: NIH RePORTER

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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. Copyright (C) 2005 by the Society for Gynecologic Investigation.

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