Cardiovascular diseases (CVDs) are the primary cause of mortality globally. The Global Burden of Disease Study indicates that CVDs account for one-third of all global deaths, with a notable 18.17% increase in their incidence over the last decade. Despite the widespread use and proven effectiveness of therapies like antiplatelet agents, lipid-lowering drugs, anticoagulants, and percutaneous coronary intervention (PCI) in managing risk factors, the long-term prognosis of patients remains suboptimal. The prevailing academic viewpoint asserts that chronic inflammation and dysregulated apoptosis lead to the accumulation of apoptotic cells or fragments, triggering inflammatory injury and oxidative stress. Efferocytosis, encompassing the recognition, engulfment, and degradation of apoptotic cells by phagocytes, is essential for preserving tissue homeostasis and limiting excessive inflammation in this context. Macrophages, being professional phagocytes, demonstrate the highest efficiency and precision in clearing apoptotic cells. Hence, this review will center on macrophage-mediated efferocytosis, systematically investigating its roles and mechanisms in the pathogenesis and progression of CVDs.
Lin et al. (Tue,) studied this question.