二十碳五烯酸诱导巨噬细胞 Mox 极化以预防糖尿病心肌病。

IF 6.5 1区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

EMBO Reports Pub Date : 2024-10-31 DOI:10.1038/s44319-024-00271-x

Jie Li, Wenshan Nan, Xiaoli Huang, Huali Meng, Shue Wang, Yan Zheng, Ying Li, Hui Li, Zhiyue Zhang, Lei Du, Xiao Yin, Hao Wu

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引用次数: 0

摘要

糖尿病心肌病（DC）会导致心力衰竭，但几乎没有有效的干预方法。二十碳五烯酸（EPA）是一种有益于心血管系统的必需营养素，但它对糖尿病心肌病的影响仍然未知。在这里，我们报告了 EPA 对链佐菌素和高脂饮食诱导的糖尿病小鼠的直流电有保护作用，重点是减少心脏 M1 极化巨噬细胞。在体外，EPA 可减轻 M1 极化巨噬细胞诱导的心肌细胞损伤，使巨噬细胞表型从 M1 极化转为 Mox 极化，而不是 M2 极化。此外，巨噬细胞的 Mox 极化还能对抗 M1 极化巨噬细胞诱导的心肌细胞损伤。此外，研究还发现血红素加氧酶1（HO-1）能维持Mox表型，介导EPA抑制巨噬细胞M1极化和随之而来的心肌细胞损伤。机理研究显示，G 蛋白偶联受体 120 介导了 EPA 对 HO-1 的上调。值得注意的是，EPA 能促进糖尿病患者单核巨噬细胞的 Mox 极化。目前的研究提供了 EPA 和巨噬细胞 Mox 极化作为直流电干预的新策略。

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Eicosapentaenoic acid induces macrophage Mox polarization to prevent diabetic cardiomyopathy.

Diabetic cardiomyopathy (DC) leads to heart failure, with few effective approaches for its intervention. Eicosapentaenoic acid (EPA) is an essential nutrient that benefits the cardiovascular system, but its effect on DC remains unknown. Here, we report that EPA protects against DC in streptozotocin and high-fat diet-induced diabetic mice, with an emphasis on the reduction of cardiac M1-polarized macrophages. In vitro, EPA abrogates cardiomyocyte injury induced by M1-polarized macrophages, switching macrophage phenotype from M1 to Mox, but not M2, polarization. Moreover, macrophage Mox polarization combats M1-polarized macrophage-induced cardiomyocyte injury. Further, heme oxygenase 1 (HO-1) was identified to maintain the Mox phenotype, mediating EPA suppression of macrophage M1 polarization and the consequential cardiomyocyte injury. Mechanistic studies reveal that G-protein-coupled receptor 120 mediates the upregulation of HO-1 by EPA. Notably, EPA promotes Mox polarization in monocyte-derived macrophages from diabetic patients. The current study provides EPA and macrophage Mox polarization as novel strategies for DC intervention.

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来源期刊

EMBO Reports 生物-生化与分子生物学

CiteScore

11.20

自引率

1.30%

发文量

267

审稿时长

1 months

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