Diabetic cardiomyopathy (DCM) as the severe complication has become the main cause of death in diabetic patients. It is supposed that macrophages participate in the inflammatory response and play a key role in the initiation and progression of DCM. Two phenotypes, M1(classically activated) macrophages and M2 (alternatively activated)macrophages, cooperate in modulating immunity and inflammation. The polarization of macrophages is influenced by autoimmunity and inflammation directly. Various inflammatory modulators, signaling pathways and transcription factors are involved in regulating macrophage polarization. When DCM occurs, local and systemic microenvironment changed, and the balance between M1 and M2 macrophages is ruined which in turn aggravating inflammation. Therefore, it has great prospect of clinical application to explore effective intervention on macrophage polarization and study the interactions between signaling pathway and progression or recovery of disease. Following is a review of role of macrophage polarization in progression and repair of DCM, for seeking a new therapeutic target of DCM.%糖尿病心肌病(diabetic cardiomyopathy,DCM)是导致糖尿病患者死亡的主要原因,而巨噬细胞参与的炎症反应在DCM的发生及发展中起到至关重要的作用.巨噬细胞的两种主要亚型—经典活化的M1型和选择活化的M2型,在炎症疾病中起到重要的免疫调节作用.机体炎症的程度及自身免疫炎症反应直接影响巨噬细胞的极化,并通过特定的信号通路及分子进行极化.DCM发生时,处于动态平衡的巨噬细胞M1/M2被打破,M1/M2比例失衡,M1促炎巨噬细胞不断增多加重炎症疾病的进展,因此有效干预巨噬细胞M2型极化使M1/M2处于平衡状态有利于促进炎症消退及组织修复,可能促进炎症的心肌细胞及内皮细胞修复.针对巨噬细胞极化分子机制的新型治疗措施有利于预防DCM的发生发展,阻止甚至逆转心功能恶化,具有重要的临床意义.本文对巨噬细胞极化在糖尿病心肌病的发生发展及心肌修复中的作用进行综述,以期寻找DCM治疗新的靶点.
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