The phagocytic role of macrophage following myocardial infarction

Myocardial infarction (MI) is one of the cardiovascular diseases with high morbidity and mortality. MI causes large amounts of apoptotic and necrotic cells that need to be efficiently and instantly engulfed by macrophage to avoid second necrosis. Phagocytic macrophages can dampen or resolve inflammation to protect infarcted heart. Phagocytosis of macrophages is modulated by various factors including proteins, receptors, lncRNA and cytokines. A better understanding of mechanisms in phagocytosis will be beneficial to regulate macrophage phagocytosis capability towards a desired direction in cardioprotection after MI. In this review, we describe the phagocytosis effect of macrophages and summarize the latest reported signals regulating phagocytosis after MI, which will provide a new thinking about phagocytosis-dependent cardiac protection after MI.

Automated summary

Myocardial infarction (MI) is a cardiovascular disease that has a high incidence and mortality rate. The disease results in a large number of apoptotic and necrotic cells that need to be efficiently and quickly engulfed by macrophages to prevent further necrosis. Phagocytic macrophages can reduce or resolve inflammation and protect the infarcted heart. The phagocytosis of macrophages is influenced by various factors such as proteins, receptors, lncRNA, and cytokines. Understanding the mechanisms of phagocytosis can help regulate macrophage phagocytic ability for cardioprotection after MI. This review provides an overview of the phagocytic effect of macrophages and summarizes the latest reported signals that regulate phagocytosis after MI, offering new insights into phagocytosis-dependent cardiac protection after MI.