Title:The Role of METTL3 in the Progression of Cardiac Fibrosis
Volume: 23
Issue: 26
Author(s): Samir Bolívar, Marian Pérez-Cantillo, Jassiris Monterroza-Torres, César Vásquez-Trincado, Jairo Castellar-Lopez and Evelyn Mendoza-Torres*
Affiliation:
- Faculty of Health Sciences, Universidad Libre Seccional Barranquilla, Barranquilla, Colombia
Keywords:
Cardiac myofibroblasts, METTL3, Cardiac remodeling, Cardiac fibrosis, Extracellular matrix, N6-methyladenosine.
Abstract: Cardiac fibrosis is known as the expansion of the cardiac interstitium through excessive
deposition of extracellular matrix proteins; this process is performed by a multifunctional cell
known as the cardiac fibroblast. After the myocardial injury, these cells are activated as a repair
program, increase, and switch to a contractile phenotype, which is evidenced by an increase in alpha-
smooth muscle actin. Likewise, there is an increase in type I and III collagen, which are considered
profibrotic biomarkers. It is believed that one of the proteins involved in cardiac remodeling is
METTL3, which is the enzyme responsible for N6-methyladenosine (m6A) methylation, the most
common and abundant epigenetic modification of eukaryotic mRNA. This review focuses on recent
studies in which the possible role of METTL3 in the progression of fibrosis has been demonstrated,
mainly in cardiac fibrogenesis.