title: Maternal inflammation, growth retardation, and preterm birth: insights into adult cardiovascular disease.
abstract: The "fetal origin of adult disease Hypothesis" originally described by Barker et al. identified the relationship between impaired in utero growth and adult cardiovascular disease risk and death. Since then, numerous clinical and experimental studies have confirmed that early developmental influences can lead to cardiovascular, pulmonary, metabolic, and psychological diseases during adulthood with and without alterations in birth weight. This so called "fetal programming" includes developmental disruption, immediate adaptation, or predictive adaptation and can lead to epigenetic changes affecting a specific organ or overall health. The intrauterine environment is dramatically impacted by the overall maternal health. Both premature birth or low birth weight can result from a variety of maternal conditions including undernutrition or dysnutrition, metabolic diseases, chronic maternal stresses induced by infections and inflammation, as well as hypercholesterolemia and smoking. Numerous animal studies have supported the importance of both maternal health and maternal environment on the long term outcomes of the offspring. With increasing rates of obesity and diabetes and survival of preterm infants born at early gestational ages, the need to elucidate mechanisms responsible for programming of adult cardiovascular disease is essential for the treatment of upcoming generations.
authors.affiliation: The Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, The Ohio State University, Columbus, Ohio, USA.
authors.forename: Lynette K
authors.initials: LK
authors.lastname: Rogers
authors.forename: Markus
authors.initials: M
authors.lastname: Velten
mesh_terms: D000328:Adult; D000818:Animals; D002318:Cardiovascular Diseases / Q000196:embryology / Q000209:etiology*; D005260:Female; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007249:Inflammation / Q000150:complications / Q000276:immunology; D011247:Pregnancy; D047928:Premature Birth / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics / Q000276:immunology; D055815:Young Adult