Abstract
Rapid and effective clearance of apoptotic cells, known as efferocytosis, is essential for maintaining tissue homeostasis. Efferocytosis removes apoptotic cells before the occurrence of membrane rupture from which the cell contents, often inflammatory and toxic, are released into surrounding tissues. Through this way, efferocytosis protects the surrounding tissues from toxic enzymes and oxides inside the apoptotic cells as well as from cellular contents such as anti-proteinase and cystatins. Driven by the ongoing advancements in bioinformatics and molecular biology, many researchers have explored the mechanism of efferocytosis and its association with systemic diseases. Multiple studies have demonstrated that impaired efferocytosis mechanisms significantly contribute to the onset and progression of chronic inflammation. The presence of chronic inflammation significantly exacerbates the advancement of cardiovascular diseases, including atherosclerosis, myocardial infarction, heart failure subsequent to myocardial infarction, and even myocarditis. This review aims to provide a brief introduction to the mechanisms involved in cellular efferocytosis, followed by an examination of the molecular and pathway aspects of efferocytosis with the risk of cardiovascular diseases, contributing to the identification of potential therapeutic targets for related diseases.