Macrophage-to-myofibroblast transition and its role in cardiac fibrosis.

After acute myocardial infarction, the heart mainly relies on fibrosis remodeling repair to maintain the structural and functional integrity of the heart, however, excessive fibrosis is an important cause of heart failure. Macrophages play an important regulatory role in cardiac fibrosis and have been found to transform into myofibroblasts through their own phenotype. Based on the existing evidence and previous research results, we summarizes the potential and mechanism of macrophage-to-myofibroblast transition (MMT) in cardiac fibrosis. Notwithstanding the burgeoning interest in MMT within the context of cardiac tissue, research in this domain remains nascent. A deeper comprehension of this phenomenon, alongside its molecular substratum, stands as a quintessential prerequisite for the demarcation of molecular targets conducive to the amelioration of cardiac fibrosis.