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Hypoxia: From Placental Development to Fetal Programming.
Fajersztajn, Lais; Veras, Mariana Matera.
Afiliación
  • Fajersztajn L; LIM 05 Departamento de Patologia, Hospital da Clinicas, Faculdade de Medicina Universidade de Sao Paulo, Sao Paulo, SP, Brasil.
  • Veras MM; LIM 05 Departamento de Patologia, Hospital da Clinicas, Faculdade de Medicina Universidade de Sao Paulo, Sao Paulo, SP, Brasil.
Birth Defects Res ; 109(17): 1377-1385, 2017 Oct 16.
Article en En | MEDLINE | ID: mdl-29105382
ABSTRACT
Hypoxia may influence normal and different pathological processes. Low oxygenation activates a variety of responses, many of them regulated by hypoxia-inducible factor 1 complex, which is mostly involved in cellular control of O2 consumption and delivery, inhibition of growth and development, and promotion of anaerobic metabolism. Hypoxia plays a significant physiological role in fetal development; it is involved in different embryonic processes, for example, placentation, angiogenesis, and hematopoiesis. More recently, fetal hypoxia has been associated directly or indirectly with fetal programming of heart, brain, and kidney function and metabolism in adulthood. In this review, the role of hypoxia in fetal development, placentation, and fetal programming is summarized. Hypoxia is a basic mechanism involved in different pregnancy disorders and fetal health developmental complications. Although there are scientific data showing that hypoxia mediates changes in the growth trajectory of the fetus, modulates gene expression by epigenetic mechanisms, and determines the health status later in adulthood, more mechanistic studies are needed. Furthermore, if we consider that intrauterine hypoxia is not a rare event, and can be a consequence of unavoidable exposures to air pollution, nutritional deficiencies, obesity, and other very common conditions (drug addiction and stress), the health of future generations may be damaged and the incidence of some diseases will markedly increase as a consequence of disturbed fetal programming. Birth Defects Research 1091377-1385, 2017.© 2017 Wiley Periodicals, Inc.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Placentación / Desarrollo Fetal / Hipoxia Límite: Female / Humans / Pregnancy Idioma: En Revista: Birth Defects Res Año: 2017 Tipo del documento: Article País de afiliación: Brasil

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Placentación / Desarrollo Fetal / Hipoxia Límite: Female / Humans / Pregnancy Idioma: En Revista: Birth Defects Res Año: 2017 Tipo del documento: Article País de afiliación: Brasil