Healthcare Pharmacy and Pharmacology Research Group, Faculty of Chemistry and Pharmacy, Universidad del Atlántico, Barranquilla, Colombia.
Center for Pharmaceutical Services and Drug Monitoring (CESFAR), Universidad del Atlántico, Barranquilla, Colombia.
Curr Top Med Chem. 2023;23(26):2427-2435. doi: 10.2174/1568026623666230825144949.
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.
心肌纤维化是指通过细胞外基质蛋白的过度沉积使心脏间质扩张的过程；这个过程是由一种多功能细胞——心肌成纤维细胞完成的。心肌损伤后，这些细胞作为修复程序被激活，增殖并转变为收缩表型，这表现为α-平滑肌肌动蛋白的增加。同样，I 型和 III 型胶原也会增加，它们被认为是成纤维的生物标志物。人们认为，参与心脏重构的蛋白质之一是 METTL3，它是负责 N6-甲基腺嘌呤（m6A）甲基化的酶，这是真核 mRNA 中最常见和最丰富的表观遗传修饰。本综述重点介绍了最近的研究，这些研究表明 METTL3 在纤维化的进展中可能发挥作用，主要是在心肌纤维化中。
