Chronic inflammation is a crucial inducerof diabetesvascular complications.Onereason is that high glucose easily induces macrophage activation.1 Macrophages are the principal participants in innate immunity and exist ...Chronic inflammation is a crucial inducerof diabetesvascular complications.Onereason is that high glucose easily induces macrophage activation.1 Macrophages are the principal participants in innate immunity and exist in all human tissues.In pathological vascular,infiltrated macrophages secrete inflammatory factors leading to an increase in plaque stability.?In macrophage polarization,autophagy plays an important role.Enhancement of macrophage autophagy could induce macrophage polarization from the M1 phenotype to M2 phenotype and inhibit inflammatory reactions.3 Our previous research found that high glucose condition promotes miR-32 expression and macrophage M1 polarization,4 but the mechanism of miR-32 promoting macrophage M1 polarization is unclear.In this study,we found that,under a high-glucose condition,miR-32/Mef2d/cAMP signaling promoted M1 macrophage polarization via inhibited autophagy.These results provide a theoretical and experimental basis for the prevention and treatment of T2D vascular inflammation.展开更多
基金supported by the National Natural Science Foundation of China(No.81873651)Natural Science Foundation of Hunan Province,China(No.2021JJ40490,2021JJ70113)Scientific Research Fund Project of Hunan Provincial Health Commission,China(No.20201981,20201901)。
文摘Chronic inflammation is a crucial inducerof diabetesvascular complications.Onereason is that high glucose easily induces macrophage activation.1 Macrophages are the principal participants in innate immunity and exist in all human tissues.In pathological vascular,infiltrated macrophages secrete inflammatory factors leading to an increase in plaque stability.?In macrophage polarization,autophagy plays an important role.Enhancement of macrophage autophagy could induce macrophage polarization from the M1 phenotype to M2 phenotype and inhibit inflammatory reactions.3 Our previous research found that high glucose condition promotes miR-32 expression and macrophage M1 polarization,4 but the mechanism of miR-32 promoting macrophage M1 polarization is unclear.In this study,we found that,under a high-glucose condition,miR-32/Mef2d/cAMP signaling promoted M1 macrophage polarization via inhibited autophagy.These results provide a theoretical and experimental basis for the prevention and treatment of T2D vascular inflammation.
