ArticleScientific reports2016
Prenatal inflammation-induced NF-κB dyshomeostasis contributes to renin-angiotensin system over-activity resulting in prenatally programmed hypertension in offspring.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Review
- High-fat intake during lactation ameliorates cardiac fatty acid metabolic disorders and dysfunction in mouse offspring undergoing prenatal poly (I:C) stimulation.Acta pharmacologica Sinica · 2025Article
- MicroRNA-155 targets p65 to regulate PD-L1 expression in the early pregnancy endometrium.Scientific reports · 2025Article
- Spatial transcriptomic analysis of tumor microenvironment in esophageal squamous cell carcinoma with HIV infection.Molecular cancer · 2025Article
- Prenatal inflammation exposure-programmed hypertension exhibits multi-generational inheritance via disrupting DNA methylome.Acta pharmacologica Sinica · 2022Article
- Interactions of the Brain Renin-Angiotensin-System (RAS) and Inflammation in the Sensitization of Hypertension.Frontiers in neuroscience · 2020Review
- Effect of heme oxygenase 1 and renin/prorenin receptor on oxidized low-density lipoprotein-induced human umbilical vein endothelial cells.Experimental and therapeutic medicine · 2019Article
- Dysregulation of miR-135a-5p promotes the development of rat pulmonary arterial hypertension in vivo and in vitro.Acta pharmacologica Sinica · 2019Article
- BCL6 Attenuates Proliferation and Oxidative Stress of Vascular Smooth Muscle Cells in Hypertension.Oxidative medicine and cellular longevity · 2019Article
- Parental Renovascular Hypertension-Induced Autonomic Dysfunction in Male Offspring Is Improved by Prenatal or Postnatal Treatment With Hydrogen Sulfide.Frontiers in physiology · 2019Article
- Alteration in the expression of the renin-angiotensin system in the myocardium of mice conceived by in vitro fertilization.Biology of reproduction · 2018Article
- Central nervous system neuroplasticity and the sensitization of hypertension.Nature reviews. Nephrology · 2018Review
- Article
- Maternal high-fat diet acts on the brain to induce baroreflex dysfunction and sensitization of angiotensin II-induced hypertension in adult offspring.American journal of physiology. Heart and circulatory physiology · 2018Article
- Prenatal Lipopolysaccharide Exposure Promotes Dyslipidemia in the Male Offspring Rats.Frontiers in physiology · 2018Article
- Maternal Gestational Hypertension-Induced Sensitization of Angiotensin II Hypertension Is Reversed by Renal Denervation or Angiotensin-Converting Enzyme Inhibition in Rat Offspring.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Profiling analysis of long non-coding RNAs in early postnatal mouse hearts.Scientific reports · 2017Article
- Silencing salusin-β attenuates cardiovascular remodeling and hypertension in spontaneously hypertensive rats.Scientific reports · 2017Article
- Sustained elevation of NF-κB activity sensitizes offspring of maternal inflammation to hypertension via impairing PGC-1α recovery.Scientific reports · 2016Article
- Maternal inflammation activated ROS-p38 MAPK predisposes offspring to heart damages caused by isoproterenol via augmenting ROS generation.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies involving the use of prenatally programmed hypertension have been shown to potentially contribute to prevention of essential hypertension (EH). Our previous research has demonstrated that prenatal inflammatory stimulation leads to offspring's aortic dysfunction and hypertension in pregnant Sprague-Dawley rats challenged with lipopolysaccharide (LPS). The present study found that prenatal LPS exposure led to NF-κB dyshomeostasis from fetus to adult, which was characterized by PI3K-Akt activation mediated degradation of IκBα protein and impaired NF-κB self-negative feedback loop mediated less newly synthesis of IκBα mRNA in thoracic aortas (gestational day 20, postnatal week 7 and 16). Prenatal or postnatal exposure of the IκBα degradation inhibitor, pyrollidine dithiocarbamate, effectively blocked NF-κB activation, endothelium dysfunction, and renin-angiotensin system (RAS) over-activity in thoracic aortas, resulting in reduced blood pressure in offspring that received prenatal exposure to LPS. Surprisingly, NF-κB dyshomeostasis and RAS over-activity were only found in thoracic aortas but not in superior mesenteric arteries. Collectively, our data demonstrate that the early life NF-κB dyshomeostasis induced by prenatal inflammatory exposure plays an essential role in the development of EH through triggering RAS over-activity. We conclude that early life NF-κB dyshomeostasis is a key predictor of EH, and thus, NF-κB inhibition represents an effective interventional strategy for EH prevention.
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