title: Glucocorticoid-induced fetal origins of adult hypertension: Association with epigenetic events.
abstract: Hypertension is a predominant risk factor for cardiovascular diseases and a major health care burden. Accumulating epidemiological and experimental evidence suggest that adult-onset hypertension may have its origins during early development. Upon exposure to glucocorticoids, the fetus develops hypertension, and the offspring may be programmed to continue the hypertensive trajectory into adulthood. Elevated oxidative stress and deranged nitric oxide system are not only hallmarks of adult hypertension but are also observed earlier in life. Endothelial dysfunction and remodeling of the vasculature, which are robustly associated with increased incidence of hypertension, are likely to have been pre-programmed during fetal life. Apparently, genomic, non-genomic, and epigenomic factors play a significant role in the development of hypertension, including glucocorticoid-driven effects on blood pressure. In this review, we discuss the involvement of the aforementioned participants in the pathophysiology of hypertension and suggest therapeutic opportunities for targeting epigenome modifiers, potentially for personalized medicine.
authors.affiliation: Department of Biological and Environmental Sciences, Qatar University, Doha, Qatar.
authors.forename: M Akhtar
authors.initials: MA
authors.lastname: Anwar
authors.affiliation: Department of Biological and Environmental Sciences, Qatar University, Doha, Qatar.
authors.forename: Alaaeldin I
authors.initials: AI
authors.lastname: Saleh
authors.affiliation: Qatar Biomedical Research Institute, Doha, Qatar.
authors.forename: Reem
authors.initials: R
authors.lastname: Al Olabi
authors.affiliation: Department of Health Sciences, Qatar University, Doha, Qatar.
authors.forename: Tuqa S
authors.initials: TS
authors.lastname: Al Shehabi
authors.affiliation: Department of Biological and Environmental Sciences, Qatar University, Doha, Qatar; Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon. Electronic address: ae81@qu.edu.qa.
authors.forename: Ali H
authors.initials: AH
authors.lastname: Eid
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D019175:DNA Methylation / Q000187:drug effects; D044127:Epigenesis, Genetic / Q000187:drug effects*; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005938:Glucocorticoids / Q000009:adverse effects*; D006657:Histones / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D018811:Maternal Exposure / Q000009:adverse effects*; D035683:MicroRNAs / Q000235:genetics; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011499:Protein Processing, Post-Translational / Q000187:drug effects
chemical_list: D005938:Glucocorticoids; D006657:Histones; D035683:MicroRNAs; D009569:Nitric Oxide; D042842:11-beta-Hydroxysteroid Dehydrogenases
keywords: Cardiovascular disease; Embryonic programming; Epigenetics; Glucocorticoids; Hypertension; Pharmacogenomics