Hypomethylation of the Angiotensin II Type I Receptor (&lt;b&gt;&lt;i&gt;AGTR1&lt;/i&gt;&lt;/b&gt;) Gene Along with Environmental Factors Increases the Risk for Essential Hypertension

Lin, Jiabing; Lin, Shaowei; Wu, Yihai; Wang, Xiaoxia; Wu, Siying; Li, Huangyuan

doi:10.1159/000458520

Cited by 20 publications

(12 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Notably, smoking and drinking are also important risk factors for hypertension, and both interact with DNA methylation of genes to affect the risk of EH . However, we did not observe any significant interactions in our study, although future studies with larger sample size are needed to confirm our findings.…”

Section: Discussioncontrasting

confidence: 45%

“…Increasing the methylation level of a promoter region will silence the transcription of the corresponding gene, whereas decreasing it may promote gene transcription . Aberrant gene methylation has been identified as an important contributor to the pathogenesis of EH, for example, hypomethylation of interleukin‐6 ( IL‐6 ), angiotensin II type 1 receptor ( AGTR1 ), angiotensin‐converting enzyme ( ACE ), Na+/K+/Cl− cotransporter protein 1 ( NKCC1 ), and α‐adducin ( ADD1 ), and the hypermethylation of 11β‐hydroxysteroid dehydrogenase type II ( 11β‐HSD‐2 ) …”

Section: Introductionmentioning

confidence: 99%

“…important contributor to the pathogenesis of EH, for example, hypomethylation of interleukin-6 (IL-6), 6 angiotensin II type 1 receptor (AGTR1), 7 angiotensin-converting enzyme (ACE), 8 Na+/K+/Cl− cotransporter protein 1 (NKCC1), 9 and α-adducin (ADD1), 10 and the hypermethylation of 11β-hydroxysteroid dehydrogenase type II (11β-HSD-2). 11 Serine hydroxymethyltransferase 1 (SHMT1), located on chromosome 17p11.2, is a key enzyme involved in folic acid metabolism.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Serine hydroxymethyltransferase 1 promoter hypermethylation increases the risk of essential hypertension

Wang

Ying

et al. 2018

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background Serine hydroxymethyltransferase 1 (SHMT1) is an enzyme involved in folic acid metabolism and is known to contribute to the development of hypertension. We evaluated the relationship between SHMT1 promoter methylation and essential hypertension (EH). Methods Quantitative methylation‐specific polymerase chain reaction was used to measure the SHMT1 promoter methylation level in 241 EH patients and 288 age‐ and gender‐matched healthy individuals. The diagnostic value of SHMT1 promoter hypermethylation was analyzed using a receiver operating characteristic (ROC) curve. The Gene Expression Omnibus (GEO) database and dual‐luciferase reporter assay were used to validate our findings. Results Compared with the control group, significant differences in SHMT1 promoter methylation were found in both EH and hyperhomocysteinemia groups (P < 0.001 and P = 0.029, respectively). The area under the curve of the diagnosis of SHMT1 promoter hypermethylation for EH was 0.808, with a sensitivity and specificity of 73.9% and 77.8%, respectively. The risk of SHMT1 promoter hypermethylation was significantly higher in the >65‐year group than in the ≤65‐year group (odds ratio = 3.925; 95% confidence interval = 2.141‐7.196). In addition, GEO database analysis showed that 5‐aza‐deoxycytidine increased gene expression in several carotid endothelial cell lines. A dual‐luciferase reporter assay revealed that the target sequence in the SHMT1 promoter upregulated gene expression. Conclusion Our findings indicate that SHMT1 promoter hypermethylation increases the risk of EH and may be a promising biomarker for EH.

show abstract

Section: Discussioncontrasting

confidence: 45%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Serine hydroxymethyltransferase 1 promoter hypermethylation increases the risk of essential hypertension

Wang

Ying

et al. 2018

Clinical Laboratory Analysis

View full text Add to dashboard Cite

show abstract

“…Studies show that hypomethylation mechanisms can lead to higher ACE, β‐adrenergic receptors and Na + channel expression in the hypertensive condition . In agreement with this, it was recently demonstrated that the hypo‐methylation process of the angiotensin II type I receptor (AGTR1) and interleukin‐6 gene in peripheral blood DNA, increase the risk of essential hypertension in human.…”

Section: Epigenetic Modifications: a Potential Pathway Linking Maternmentioning

confidence: 59%

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Alves

Costa‐Silva

2017

Clin Exp Pharma Physio

View full text Add to dashboard Cite

SummaryMaternal protein malnutrition during the critical stages of development (pregnancy, lactation and first infancy) can lead to adult hypertension. Studies have shown that renal and cardiovascular dysfunctions can be associated to the development of hypertension in humans and rats exposed to maternal protein malnutrition. The etiology of hypertension, however, includes a complex network involved in central and peripheral blood pressure control. Recently, the hyperactivity of the sympathetic nervous system in protein-restricted rats has been reported. Studies have shown that protein malnutrition during pregnancy and/or lactation alters blood pressure control through mechanisms that include central sympathetic-respiratory dysfunctions and epigenetic modifications, which may contribute to adult hypertension. Thus, this review will discuss the historical context, new evidences of neurogenic disruption in respiratorysympathetic activities and possible epigenetic mechanisms involved in maternal protein malnutrition induced-hypertension. K E Y W O R D Shypertension, malnutrition, phenotypic plasticity, sympathetic activity, ventilation | INTRODUCTIONArterial hypertension (AH) affects more than 1 billion people around the world and is a major risk factor for cardiovascular dysfunction, recognized as the main cause of morbidity and mortality. Because of the interaction between the sympathetic and respiratory nervous systems, growing evidence supports the notion that an increase in sympathetic and respiratory activities plays an important role in the development of hypertension. [8][9][10] This observation has prompted the development of several studies evaluating sympathetic and respiratory activities and sensitivity of peripheral and central chemoreceptors in various hypertension models. For example, in chronic intermittent hypoxia 8,11 in spontaneously hypertensive rats (SHR) 4 and in renovascular hypertension, 12 augmented sympathetic-respiratory activities and higher peripheral chemosensitivity were seen to be associated to hypertension.

show abstract

“…Lin et al reported that hypomethylation of the angiotensin II type I receptor gene correlated with higher systolic and diastolic BPs. Smokers with HTN were also observed to have a lower level of methylation ( 66 ).…”

Section: Epigenetics Of Htnmentioning

confidence: 99%

Genetic Programming of Hypertension

Ahn

Gupta

2018

Front. Pediatr.

View full text Add to dashboard Cite

The heritability of hypertension (HTN) is widely recognized and as a result, extensive studies ranging from genetic linkage analyses to genome-wide association studies are actively ongoing to elucidate the etiology of both monogenic and polygenic forms of HTN. Due to the complex nature of essential HTN, however, single genes affecting blood pressure (BP) variability remain difficult to isolate and identify and have rendered the development of single-gene targeted therapies challenging. The roles of other causative factors in modulating BP, such as gene–environment interactions and epigenetic factors, are increasingly being brought to the forefront. In this review, we discuss the various monogenic HTN syndromes and corresponding pathophysiologic mechanisms, the different methodologies employed in genetic studies of essential HTN, the mechanisms for epigenetic modulation of essential HTN, pharmacogenomics and HTN, and finally, recent advances in genetic studies of essential HTN in the pediatric population.

show abstract

Hypomethylation of the Angiotensin II Type I Receptor (<b><i>AGTR1</i></b>) Gene Along with Environmental Factors Increases the Risk for Essential Hypertension

Cited by 20 publications

References 37 publications

Serine hydroxymethyltransferase 1 promoter hypermethylation increases the risk of essential hypertension

Serine hydroxymethyltransferase 1 promoter hypermethylation increases the risk of essential hypertension

Maternal protein malnutrition induced‐hypertension: New evidence about the autonomic and respiratory dysfunctions and epigenetic mechanisms

Genetic Programming of Hypertension

Contact Info

Product

Resources

About