The COVID-19 pandemic is one of the most significant public health threats in recent history and has impacted the lives of almost everyone worldwide. Epigenetic mechanisms contribute to many aspects of the SARS-CoV-2 replication cycle, including expression levels of viral receptor ACE2, expression of cytokine genes as part of the host immune response, and the implication of various histone modifications in several aspects of COVID-19. SARS-CoV-2 proteins physically associate with many different host proteins over the course of infection, and notably there are several interactions between viral proteins and epigenetic enzymes such as HDACs and bromodomain-containing proteins as shown by correlation-based studies. The many contributions of epigenetic mechanisms to the viral life cycle and the host immune response to infection have resulted in epigenetic factors being identified as emerging biomarkers for COVID-19, and project epigenetic modifiers as promising therapeutic targets to combat COVID-19. This review article highlights the major epigenetic pathways at play during COVID-19 disease and discusses ongoing clinical trials that will hopefully contribute to slowing the spread of SARS-CoV-2.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1139/gen-2020-0135 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
New Multiomic Studies Shed Light on Cellular Diversity and Neuronal Susceptibility in Parkinson's Disease.
Mov Disord
January 2025
Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Parkinson's disease is a complex neurodegenerative disorder characterized by degeneration of dopaminergic neurons, with patients manifesting varying motor and nonmotor symptoms. Previous studies using single-cell RNA sequencing in rodent models and humans have identified distinct heterogeneity of neurons and glial cells with differential vulnerability. Recent studies have increasingly leveraged multiomics approaches, including spatial transcriptomics, epigenomics, and proteomics, in the study of Parkinson's disease, providing new insights into pathogenic mechanisms.
View Article and Find Full Text PDFUsing Multi-Omics Methods to Understand Gouty Arthritis.
Curr Rheumatol Rev
January 2025
Department of Rheumatology, Beijing Jishuitan Hospital, Guizhou Hospital, China.
Gouty arthritis is a common arthritic disease caused by the deposition of monosodium urate crystals in the joints and the tissues around it. The main pathogenesis of gout is the inflammation caused by the deposition of monosodium urate crystals. Omics studies help us evaluate global changes in gout during recent years, but most studies used only a single omics approach to illustrate the mechanisms of gout.
View Article and Find Full Text PDFGlobal Burden of Early-Onset Ischemic Heart Disease, 1990 to 2019.
JACC Adv
January 2025
Department of Endocrinology Medicine, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Background: Early-onset ischemic heart disease (IHD) is a growing burden associated with high disability and death.
Objectives: This study aimed to estimate the burden of incidence, prevalence, and disability-adjusted life years (DALY) of early-onset IHD from 1990 to 2019.
Methods: Data on the burden of early-onset IHD (men<55 years, women<65 years), including prevalence, incidence, DALY, and deaths, were collected from the Global Burden of Disease study for 204 countries and territories from 1990 to 2019.
ETV2/ER71 regulates hematovascular lineage generation and vascularization through an H3K9 demethylase, KDM4A.
iScience
January 2025
Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA.
ETV2/ER71, an ETS (E-twenty six) transcription factor, is critical for hematopoiesis and vascular development. However, research about the molecular mechanisms behind ETV2-mediated gene transcription is limited. Herein, we demonstrate that ETV2 and KDM4A, an H3K9 demethylase, regulate hematopoietic and endothelial genes.
View Article and Find Full Text PDFDNA methylation of long noncoding RNA cytochrome B in diabetic retinopathy.
Noncoding RNA Res
April 2025
Kresge Eye Institute, Wayne State University, Detroit, MI, USA.
Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc), is also downregulated.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!