The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks

Smoking could predispose individuals to a more severe COVID-19 by upregulating a particular gene known as mdig, which is mediated through a number of well-known histone modifications. Smoking might regulate the transcription-activating H3K4me3 mark, along with the transcription-repressing H3K9me3 an...

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Autor principal: Shirvaliloo, Milad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Future Medicine Ltd 2022
Materias:
Perspective
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8763212/
https://www.ncbi.nlm.nih.gov/pubmed/35021853
http://dx.doi.org/10.2217/epi-2021-0476
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author Shirvaliloo, Milad
author_facet Shirvaliloo, Milad
author_sort Shirvaliloo, Milad
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description Smoking could predispose individuals to a more severe COVID-19 by upregulating a particular gene known as mdig, which is mediated through a number of well-known histone modifications. Smoking might regulate the transcription-activating H3K4me3 mark, along with the transcription-repressing H3K9me3 and H3K27me3 marks, in a way to favor SARS-CoV-2 entry by enhancing the expression of ACE2, NRP1 and NRP2, AT1R, CTSD and CTSL, PGE2 receptors 2–4, SLC6A20 and IL-6, all of which interact either directly or indirectly with important receptors, facilitating viral entry in COVID-19.
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spelling pubmed-87632122022-01-20 The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks Shirvaliloo, Milad Epigenomics Perspective Smoking could predispose individuals to a more severe COVID-19 by upregulating a particular gene known as mdig, which is mediated through a number of well-known histone modifications. Smoking might regulate the transcription-activating H3K4me3 mark, along with the transcription-repressing H3K9me3 and H3K27me3 marks, in a way to favor SARS-CoV-2 entry by enhancing the expression of ACE2, NRP1 and NRP2, AT1R, CTSD and CTSL, PGE2 receptors 2–4, SLC6A20 and IL-6, all of which interact either directly or indirectly with important receptors, facilitating viral entry in COVID-19. Future Medicine Ltd 2022-01-13 2022-01 /pmc/articles/PMC8763212/ /pubmed/35021853 http://dx.doi.org/10.2217/epi-2021-0476 Text en © 2022 Future Medicine Ltd https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/)
spellingShingle Perspective
Shirvaliloo, Milad
The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title_full The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title_fullStr The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title_full_unstemmed The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title_short The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks
title_sort unfavorable clinical outcome of covid-19 in smokers is mediated by h3k4me3, h3k9me3 and h3k27me3 histone marks
topic Perspective
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8763212/
https://www.ncbi.nlm.nih.gov/pubmed/35021853
http://dx.doi.org/10.2217/epi-2021-0476
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