动脉粥样硬化(AS)是一种慢性炎症性血管疾病,发生在大、中动脉内膜,免疫系统受累。它是心血管疾病高发病率和高死亡率的共同病理基础。凋亡细胞和坏死细胞的异常增殖导致AS斑块扩张,坏死核形成,和破裂。在AS的早期阶段,巨噬细胞发挥有效吞噬作用,吞噬和降解凋亡,死了,损坏,或衰老细胞,从而实现对生物体的调节。在AS的早期阶段,巨噬细胞依靠这种作用来减缓AS的过程。然而,在AS的高级阶段,斑块内巨噬细胞的胞增作用受损,这导致巨噬细胞无法及时从生物体中清除凋亡细胞(AC),导致AS恶化。此外,AS斑块中CD47表达的上调也保护ACs免受巨噬细胞的吞噬,导致斑块中大量残留的ACs,进一步扩大坏死核。在这次审查中,我们讨论了在动脉粥样硬化过程中涉及的分子机制,以及在动脉粥样硬化过程中,希望为AS的治疗提供新的见解。
Atherosclerosis (AS) is a chronic inflammatory vascular disease that occurs in the intima of large and medium-sized arteries with the immune system\'s involvement. It is a common pathological basis for high morbidity and mortality of cardiovascular diseases. Abnormal proliferation of apoptotic cells and necrotic cells leads to AS plaque expansion, necrotic core formation, and rupture. In the early stage of AS, macrophages exert an efferocytosis effect to engulf and degrade apoptotic, dead, damaged, or senescent cells by efferocytosis, thus enabling the regulation of the organism. In the early stage of AS, macrophages rely on this effect to slow down the process of AS. However, in the advanced stage of AS, the efferocytosis of macrophages within the plaque is impaired, which leads to the inability of macrophages to promptly remove the apoptotic cells (ACs) from the organism promptly, causing exacerbation of AS. Moreover, upregulation of CD47 expression in AS plaques also protects ACs from phagocytosis by macrophages, resulting in a large amount of residual ACs in the plaque, further expanding the necrotic core. In this review, we discussed the molecular mechanisms involved in the process of efferocytosis and how efferocytosis is impaired and regulated during AS, hoping to provide new insights for treating AS.