Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.
N6-methyladenosine
cardiovascular diseases
epigenetics
macrophage polarization
non-coding RNAs
Journal
Pharmaceuticals (Basel, Switzerland)
ISSN: 1424-8247
Titre abrégé: Pharmaceuticals (Basel)
Pays: Switzerland
ID NLM: 101238453
Informations de publication
Date de publication:
18 Jan 2023
18 Jan 2023
Historique:
received:
26
10
2022
revised:
12
01
2023
accepted:
13
01
2023
medline:
1
6
2023
pubmed:
1
6
2023
entrez:
1
6
2023
Statut:
epublish
Résumé
Cardiovascular diseases (CVDs) are the leading cause of hospitalization and death worldwide, especially in developing countries. The increased prevalence rate and mortality due to CVDs, despite the development of several approaches for prevention and treatment, are alarming trends in global health. Chronic inflammation and macrophage infiltration are key regulators of the initiation and progression of CVDs. Recent data suggest that epigenetic modifications, such as DNA methylation, posttranslational histone modifications, and RNA modifications, regulate cell development, DNA damage repair, apoptosis, immunity, calcium signaling, and aging in cardiomyocytes; and are involved in macrophage polarization and contribute significantly to cardiac disease development. Cardiac macrophages not only trigger damaging inflammatory responses during atherosclerotic plaque formation, myocardial injury, and heart failure but are also involved in tissue repair, remodeling, and regeneration. In this review, we summarize the key epigenetic modifications that influence macrophage polarization and contribute to the pathophysiology of CVDs, and highlight their potential for the development of advanced epigenetic therapies.
Identifiants
pubmed: 37259293
pii: ph16020141
doi: 10.3390/ph16020141
pmc: PMC9963081
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Subventions
Organisme : National Natural Science Foundation of China
ID : 82270287
Organisme : National Natural Science Foundation of China
ID : 81670311
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