Artikel ; Online: 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.
International journal of environmental research and public health
2019 Band 16, Heft 23
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. ... ...
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 ( |
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Mesh-Begriff(e) | DNA Methylation ; Essential Hypertension/genetics ; Female ; Genotype ; Humans |
Sprache | Englisch |
Erscheinungsdatum | 2019-12-01 |
Erscheinungsland | Switzerland |
Dokumenttyp | Journal Article ; Systematic Review |
ISSN | 1660-4601 |
ISSN (online) | 1660-4601 |
DOI | 10.3390/ijerph16234829 |
Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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