Foetal hypoxia increases cardiac AT(2)R expression and subsequent vulnerability to adult ischaemic injury.
about
Role of endothelin in uteroplacental circulation and fetal vascular functionFetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: mechanisms and possible interventionsAdverse perinatal environment contributes to altered cardiac development and function.Developmental programming of cardiovascular dysfunction by prenatal hypoxia and oxidative stressGlucocorticoid modulates angiotensin II receptor expression patterns and protects the heart from ischemia and reperfusion injury.Angiotensin II receptors and drug discovery in cardiovascular disease.Newborn hypoxia/anoxia inhibits cardiomyocyte proliferation and decreases cardiomyocyte endowment in the developing heart: role of endothelin-1.Maternal hypoxia alters matrix metalloproteinase expression patterns and causes cardiac remodeling in fetal and neonatal ratsDexamethasone Treatment of Newborn Rats Decreases Cardiomyocyte Endowment in the Developing Heart through Epigenetic ModificationsFetal hypoxia and programming of matrix metalloproteinases.Chronic Losartan Treatment Up-Regulates AT1R and Increases the Heart Vulnerability to Acute Onset of Ischemia and Reperfusion Injury in Male Rats.Pre-eclampsia and offspring cardiovascular health: mechanistic insights from experimental studies.Maternal Dexamethasone Treatment Alters Tissue and Circulating Components of the Renin-Angiotensin System in the Pregnant Ewe and Fetus.Normal lactational environment restores cardiomyocyte number after uteroplacental insufficiency: implications for the preterm neonatePerinatal nicotine exposure increases vulnerability of hypoxic-ischemic brain injury in neonatal rats: role of angiotensin II receptors.Fetal programming of the neuroendocrine-immune system and metabolic disease.Developmental nicotine exposure results in programming of alveolar simplification and interstitial pulmonary fibrosis in adult male rats.Estrogen Regulates Angiotensin II Receptor Expression Patterns and Protects the Heart from Ischemic Injury in Female Rats.Antenatal hypoxia induces epigenetic repression of glucocorticoid receptor and promotes ischemic-sensitive phenotype in the developing heart.Thyroid hormone is required for growth adaptation to pressure load in the ovine fetal heartRole of the hypothalamic-pituitary-adrenal axis in developmental programming of health and disease.Hypoxia inhibits cardiomyocyte proliferation in fetal rat hearts via upregulating TIMP-4Promoter methylation represses AT2R gene and increases brain hypoxic-ischemic injury in neonatal ratsEndothelin-1 promotes cardiomyocyte terminal differentiation in the developing heart via heightened DNA methylation.Fetal hypoxia increases vulnerability of hypoxic-ischemic brain injury in neonatal rats: role of glucocorticoid receptors.Early origins of heart disease: low birth weight and the role of the insulin-like growth factor system in cardiac hypertrophy.Non-genomic effect of glucocorticoids on cardiovascular system.Developmental programming of cardiovascular disease by prenatal hypoxia.Ischemia/Reperfusion.Hypoxia-induced proliferation in mesenchymal stem cells and angiotensin II-mediated PI3K/AKT pathway.Renin-Angiotensin system hyperactivation can induce inflammation and retinal neural dysfunction.Maternal High-Fat Diet Causes a Sex-Dependent Increase in AGTR2 Expression and Cardiac Dysfunction in Adult Male Rat Offspring.An Intronic Enhancer Element Regulates Angiotensin II Type 2 Receptor Expression during Satellite Cell Differentiation, and Its Activity Is Suppressed in Congestive Heart Failure.MicroRNA-210 suppresses glucocorticoid receptor expression in response to hypoxia in fetal rat cardiomyocytes.Recombinant Relaxin Protects Liver Transplants from Ischemia Damage via Hepatocyte Glucocorticoid Receptor: From Bench-to-Bedside.SIRT1 increases cardiomyocyte binucleation in the heart development.Impaired myocardial development resulting in neonatal cardiac hypoplasia alters postnatal growth and stress response in the heart.Growth restriction in the rat alters expression of cardiac JAK/STAT genes in a sex-specific manner.The detrimental effects of glucocorticoids exposure during pregnancy on offspring's cardiac functions mediated by hypermethylation of bone morphogenetic protein-4
P2860
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P2860
Foetal hypoxia increases cardiac AT(2)R expression and subsequent vulnerability to adult ischaemic injury.
description
2010 nî lūn-bûn
@nan
2010 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Foetal hypoxia increases cardiac AT
@nl
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@ast
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@en
type
label
Foetal hypoxia increases cardiac AT
@nl
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@ast
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@en
prefLabel
Foetal hypoxia increases cardiac AT
@nl
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@ast
Foetal hypoxia increases cardi ...... ity to adult ischaemic injury.
@en
P2093
P2860
P356
P1476
Foetal hypoxia increases cardi ...... lity to adult ischaemic injury
@en
P2093
Chiranjib Dasgupta
P2860
P304
P356
10.1093/CVR/CVQ303
P50
P577
2010-09-23T00:00:00Z