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Novel methylation mark and essential hypertension

BACKGROUND: Essential hypertension (EH) is an important risk factor for various cardiovascular, cerebral and renal disorders. It is a multi-factorial trait which occurs through complex interplay between genetic, epigenetic, and environmental factors. Even after advancement of technology and decipher...

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Autor principal: Chaudhary, Mayank
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8777530/
https://www.ncbi.nlm.nih.gov/pubmed/35061109
http://dx.doi.org/10.1186/s43141-022-00301-y
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author Chaudhary, Mayank
author_facet Chaudhary, Mayank
author_sort Chaudhary, Mayank
collection PubMed
description BACKGROUND: Essential hypertension (EH) is an important risk factor for various cardiovascular, cerebral and renal disorders. It is a multi-factorial trait which occurs through complex interplay between genetic, epigenetic, and environmental factors. Even after advancement of technology and deciphering the involvement of multiple signalling pathways in blood pressure regulation, it still remains as a huge global concern. MAIN BODY OF THE ABSTRACT: Genome-wide association studies (GWAS) have revealed EH-associated genetic variants but these solely cannot explain the variability in blood pressure indicating the involvement of additional factors. The etiopathogenesis of hypertension has now advanced to the level of epigenomics where aberrant DNA methylation is the most defined epigenetic mechanism to be involved in gene regulation. Though role of DNA methylation in cancer and other mechanisms is deeply studied but this mechanism is in infancy in relation to hypertension. Generally, 5-methylcytosine (5mC) levels are being targeted at both individual gene and global level to find association with the disease. But recently, with advanced sequencing techniques another methylation mark, N6-methyladenine (6mA) was found and studied in humans which was earlier considered to be absent in case of eukaryotes. Relation of aberrant 6mA levels with cancer and stem cell fate has drawn attention to target 6mA levels with hypertension too. CONCLUSION: Recent studies targeting hypertension has suggested 6mA levels as novel marker and its demethylase, ALKBH1 as probable therapeutic target to prevent hypertension through epigenetic programming. This review compiles different methylation studies and suggests targeting of both 5mC and 6mA levels to cover role of methylation in hypertension in broader scenario.
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spelling pubmed-87775302022-02-04 Novel methylation mark and essential hypertension Chaudhary, Mayank J Genet Eng Biotechnol Review BACKGROUND: Essential hypertension (EH) is an important risk factor for various cardiovascular, cerebral and renal disorders. It is a multi-factorial trait which occurs through complex interplay between genetic, epigenetic, and environmental factors. Even after advancement of technology and deciphering the involvement of multiple signalling pathways in blood pressure regulation, it still remains as a huge global concern. MAIN BODY OF THE ABSTRACT: Genome-wide association studies (GWAS) have revealed EH-associated genetic variants but these solely cannot explain the variability in blood pressure indicating the involvement of additional factors. The etiopathogenesis of hypertension has now advanced to the level of epigenomics where aberrant DNA methylation is the most defined epigenetic mechanism to be involved in gene regulation. Though role of DNA methylation in cancer and other mechanisms is deeply studied but this mechanism is in infancy in relation to hypertension. Generally, 5-methylcytosine (5mC) levels are being targeted at both individual gene and global level to find association with the disease. But recently, with advanced sequencing techniques another methylation mark, N6-methyladenine (6mA) was found and studied in humans which was earlier considered to be absent in case of eukaryotes. Relation of aberrant 6mA levels with cancer and stem cell fate has drawn attention to target 6mA levels with hypertension too. CONCLUSION: Recent studies targeting hypertension has suggested 6mA levels as novel marker and its demethylase, ALKBH1 as probable therapeutic target to prevent hypertension through epigenetic programming. This review compiles different methylation studies and suggests targeting of both 5mC and 6mA levels to cover role of methylation in hypertension in broader scenario. Springer Berlin Heidelberg 2022-01-21 /pmc/articles/PMC8777530/ /pubmed/35061109 http://dx.doi.org/10.1186/s43141-022-00301-y Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review
Chaudhary, Mayank
Novel methylation mark and essential hypertension
title Novel methylation mark and essential hypertension
title_full Novel methylation mark and essential hypertension
title_fullStr Novel methylation mark and essential hypertension
title_full_unstemmed Novel methylation mark and essential hypertension
title_short Novel methylation mark and essential hypertension
title_sort novel methylation mark and essential hypertension
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8777530/
https://www.ncbi.nlm.nih.gov/pubmed/35061109
http://dx.doi.org/10.1186/s43141-022-00301-y
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