dc.creatorChao, Yung-Mei
dc.creatorChan, Julie Y.H.
dc.date2020-06
dc.date2021-10-05T14:44:35Z
dc.date.accessioned2023-07-15T03:39:40Z
dc.date.available2023-07-15T03:39:40Z
dc.identifierhttp://sedici.unlp.edu.ar/handle/10915/126221
dc.identifierhttps://pmr.safisiol.org.ar/archive/id/119
dc.identifierissn:1669-5410
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/7466560
dc.descriptionCardiometabolic syndrome (CMS) is now a disease entity recognized by the World Health Organization. Emerging evidence from both human epidemiological and animal studies indicates that adult CMS may have its origins in early life and can be programmed by intrauterine and early postnatal environments; a phenomenon known as fetal programming of adult disease. This mini-review discusses [1]how exposures to various insults from the mother during gestation and/or lactation programs the fetus that prompts the development of CMS during adulthood; [2] what are the currently known underlying mechanisms, with emphasis on the role of tissue oxidative stress; and [3] whether CMS in the offspring can be reprogrammed via targeting maternal tissue oxidative stress. Translational perspective of the research field is also discussed.
dc.descriptionSociedad Argentina de Fisiología
dc.formatapplication/pdf
dc.format24-33
dc.languageen
dc.rightshttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.rightsCreative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.subjectCiencias Médicas
dc.subjectFetal programming
dc.subjectOxidative stress
dc.subjectCardiometabolic syndrome
dc.subjectReprogramming therapy
dc.subjectAntioxidants
dc.titleOxidative stress in fetal programming of cardiometabolic syndrome
dc.typeArticulo
dc.typeArticulo


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