The unfavorable clinical outcome of COVID-19 in smokers is mediated by H3K4me3, H3K9me3 and H3K27me3 histone marks.
Epigenomics
; 14(3): 153-162, 2022 02.
Article
in English
| MEDLINE | ID: covidwho-1622527
ABSTRACT
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.
Lay abstract The role of smoking in development of several respiratory diseases has been clearly established. A significant proportion of these deleterious effects is mediated through epigenetic mechanisms, particularly histone modifications. Recent evidence indicates that smoking induces the expression of a mediator known as mdig, which in turn alters the transcription of several key proteins that have been implicated in development of COVID-19.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Nuclear Proteins
/
Histones
/
Smoking
/
Protein Processing, Post-Translational
/
Epigenesis, Genetic
/
Dioxygenases
/
Histone Demethylases
/
COVID-19
Type of study:
Diagnostic study
/
Prognostic study
Topics:
Variants
Language:
English
Journal:
Epigenomics
Year:
2022
Document Type:
Article
Affiliation country:
Epi-2021-0476
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