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Mechanism of efferocytosis in atherosclerosis
Li-Xia Shu1,2, Liu-Li Cao1,2, Xin Guo1,2
1Institute of Pharmacy and Pharmacology, School of Pharmaceutical Sciences, Hengyang Medical School, University of South China, Hengyang, 421001, China.
Insights
Macrophages normally clear dead cells in atherosclerosis (AS). Impaired efferocytosis and CD47 upregulation in advanced AS lead to cell buildup, worsening the disease and necrotic core expansion.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cellular Biology
Background:
- Atherosclerosis (AS) is a chronic inflammatory vascular disease linked to cardiovascular morbidity and mortality.
- Abnormal cell proliferation and accumulation drive AS plaque expansion, necrotic core formation, and rupture.
- Macrophages play a critical role in regulating AS through efferocytosis, the process of clearing apoptotic and necrotic cells.
Purpose of the Study:
- To review the molecular mechanisms of efferocytosis in atherosclerosis.
- To discuss how efferocytosis becomes impaired during AS progression.
- To explore regulatory mechanisms of efferocytosis for potential therapeutic insights.
Main Methods:
- Literature review of molecular mechanisms in efferocytosis.
- Analysis of macrophage function and efferocytosis in early versus advanced AS.
- Examination of CD47's role in protecting apoptotic cells from phagocytosis.
Main Results:
- In early AS, macrophages effectively clear apoptotic cells (ACs) via efferocytosis, slowing disease progression.
- In advanced AS, macrophage efferocytosis is impaired, leading to delayed AC removal.
- Upregulated CD47 on AS plaques inhibits macrophage phagocytosis of ACs, expanding the necrotic core.
Conclusions:
- Impaired efferocytosis and CD47 upregulation are key factors in AS exacerbation.
- Understanding these mechanisms offers potential targets for novel AS treatments.
- Restoring efferocytosis may be a promising therapeutic strategy for atherosclerosis.
Abstract:
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.
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