Fig. 7 | International Journal of Oral Science

Fig. 7

From: Oral pathogen aggravates atherosclerosis by inducing smooth muscle cell apoptosis and repressing macrophage efferocytosis

Fig. 7

Model of P. gingivalis-induced immune subversion in atherosclerosis and the underlying therapeutical strategy. P. gingivalis that is orally implanted in the periodontal pockets can transfer into the blood circulation and ultimately colonize in inflammatory vascular sites. After crossing the endothelial cell layer, P. gingivalis facilitates SMCs apoptosis and extracellular release of apoEVs-miR-143/145. These apoEVs containing large amounts of miR-143/145 are captured by macrophages and trigger blocked efferocytosis by transcriptional enhancing Siglec-G expression to activate the anti-phagocytic signal, leading to accumulated apoptotic SMCs. To therapeutically kill bacteria and remove apoptotic SMCs, MM/SMNPs nanoparticles are developed and demonstrated to efficiently target P. gingivalis-infected periodontium and atherosclerosis, which subsequently exerts bactericidal effect and restores macrophage efferocytosis

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