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Showing content from https://pubmed.ncbi.nlm.nih.gov/31805646/ below:

DNA Methylation of Candidate Genes (ACE II, IFN-γ, AGTR 1, CKG, ADD1, SCNN1B and TLR2) in Essential Hypertension: A Systematic Review and Quantitative Evidence Synthesis

. 2019 Dec 1;16(23):4829. doi: 10.3390/ijerph16234829. DNA Methylation of Candidate Genes (ACE II, IFN-γ, AGTR 1, CKG, ADD1, SCNN1B and TLR2) in Essential Hypertension: A Systematic Review and Quantitative Evidence Synthesis

Affiliations

¹ Nemours/A.I. DuPont Children's Hospital, Nemours Office of Health Equity & Inclusion, 2200 Concord Pike, 7th Floor, Wilmington, DE 19803, USA.
² Biological Sciences Department, University of Delaware, Newark, DE 19711, USA.
³ Institute of Public Health, Florida A&M University, Tallahassee, FL 32301, USA.

PMID: 31805646
PMCID: PMC6926644
DOI: 10.3390/ijerph16234829

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DNA Methylation of Candidate Genes (ACE II, IFN-γ, AGTR 1, CKG, ADD1, SCNN1B and TLR2) in Essential Hypertension: A Systematic Review and Quantitative Evidence Synthesis

Laurens Holmes Jr et al. Int J Environ Res Public Health. 2019.

. 2019 Dec 1;16(23):4829. doi: 10.3390/ijerph16234829. Affiliations

¹ Nemours/A.I. DuPont Children's Hospital, Nemours Office of Health Equity & Inclusion, 2200 Concord Pike, 7th Floor, Wilmington, DE 19803, USA.
² Biological Sciences Department, University of Delaware, Newark, DE 19711, USA.
³ Institute of Public Health, Florida A&M University, Tallahassee, FL 32301, USA.

PMID: 31805646
PMCID: PMC6926644
DOI: 10.3390/ijerph16234829

Item in Clipboard

Abstract

Physical, chemical, and social environments adversely affect the molecular process and results in cell signal transduction and the subsequent transcription factor dysregulation, leading to impaired gene expression and abnormal protein synthesis. Stressful environments such as social adversity, isolation, sustained social threats, physical inactivity, and highly methylated diets predispose individuals to molecular level alterations such as aberrant epigenomic modulations that affect homeostasis and hemodynamics. With cardiovascular disease as the leading cause of mortality in the US and blacks/African Americans being disproportionately affected by hypertension (HTN) which contributes substantially to these deaths, reflecting the excess mortality and survival disadvantage of this sub-population relative to whites, understanding the molecular events, including epigenomic and socio-epigenomic modulations, is relevant to narrowing the black-white mortality risk differences. We aimed to synthesize epigenomic findings in HTN namely (a) angiotensin-converting enzyme 2 (ACE II) gene, (b) Toll-like receptor 2 (TLR2) gene, (c) interferon γ (IFN-γ) gene, and (d) Capping Actin Protein, Gelosin-Like (CAPG) gene, adducin 1(ADD1) gene, (e) Tissue inhibitor of metalloproteinase 3 (TIMP3), (f) mesoderm specific transcript (MEST) loci, (g) sodium channel epithelial 1 alpha subunit 2 (SCNN1B), (h) glucokinase (CKG) gene (i) angiotensin II receptor, type1 (AGTR1), and DNA methylation (mDNA). A systematic review and quantitative evidence synthesis (QES) was conducted using Google Scholar and PubMed with relevant search terms. Data were extracted from studies on: (a) Epigenomic modulations in HTN based on ACE II (b) TLR2, (c) IFN-γ gene, (d) CAPG, ADD1, TIMP3, MEST loci, and mDNA. The random-effect meta-analysis method was used for a pooled estimate of the common effect size, while z statistic and I^2 were used for the homogeneity of the common effect size and between studies on heterogeneity respectively. Of the 642 studies identified, five examined hypermethylation while seven studies assessed hypomethylation in association with HTN. The hypermethylation of ACE II, SCNN1B, CKG, IFN-γ gene, and miR-510 promoter were associated with hypertension, the common effect size (CES) = 6.0%, 95% CI, -0.002-11.26. In addition, the hypomethylation of TLR2, IFN-γ gene, ADD1, AGTR1, and GCK correlated with hypertension, the CES = 2.3%, 95% CI, -2.51-7.07. The aberrant epigenomic modulation of ACE II, TLR2, IFN-γ, AGTR1, and GCK correlated with essential HTN. Transforming the environments resulting from these epigenomic lesions will facilitate early intervention mapping in reducing HTN in the US population, especially among socially disadvantaged individuals, particularly racial/ethnic minorities.

Keywords: DNA methylation and hypertension; epigenomics; essential hypertension; hypertension candidate genes; socio-epigenomics.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures
Figure 1

DNA methylation and hypertension (HTN).

Figure 1

DNA methylation and hypertension (HTN).

Figure 1

DNA methylation and hypertension (HTN).

Figure 2

Hypomethylation of candidate genes in…

Figure 2

Hypomethylation of candidate genes in essential hypertension. Notes and abbreviations: Random effect meta-analysis…

Figure 2

Hypomethylation of candidate genes in essential hypertension. Notes and abbreviations: Random effect meta-analysis with meta-regression for sub-gene common effect size estimation. cytosine-phosphate-guanine = CpG. The heterogeneity test for a single gene mDNA is not quantified and represented as .%, and p = .

Figure 3

Hyper or dense methylation of…

Figure 3

Hyper or dense methylation of candidate genes in essential hypertension. Notes and abbreviations:…

Figure 3

Hyper or dense methylation of candidate genes in essential hypertension. Notes and abbreviations: Random effect meta-analysis with meta-regression for sub-gene common effect size estimation. cytosine-phosphate-guanine = CpG. The heterogeneity test for a single gene mDNA is not quantified and represented as .%, and p = .