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. Author manuscript; available in PMC: 2017 Jun 5.
Published in final edited form as: Circ J. 2016 Oct 8;80(11):2259–2268. doi: 10.1253/circj.CJ-16-0924

Figure 4.

Figure 4

Physiological macrophage efferocytosis in atherosclerotic lesions involves a number of efferocytotic receptors, bridging molecules, and apoptotic cell ligands. The efferocytosis receptor complexes that affect atherosclerosis development in mice include SR-BI, TG2-αvβ3, MERTK-αvβ5, and LRP1-CRT-ABCA7. SR-BI interaction with apoptotic cell phosphatidylserine (PS) stimulates Src membrane recruitment and phosphorylation, leading to downstream activation of phosphoinositide 3-kinase and Rac1 to promote formation of the phagocytic cup and efficient efferocytosis. Efferocytosis by SR-BI and the other receptors stimulates anti-inflammatory signaling and promotes phagocyte survival. In advanced atherosclerotic lesions, enhanced oxidative stress and inflammation leads to defective efferocytosis, resulting in secondary necrotic death, heightened inflammation, and cytotoxicity.