Dectin-1 deficiency alleviates diabetic cardiomyopathy by attenuating macrophage-mediated inflammatory response

被引:8
作者
Yang, Na [1 ,2 ,3 ]
Wang, Minxiu [3 ]
Lin, Ke [3 ]
Wang, Mengyang [3 ]
Xu, Diyun [1 ,2 ,3 ]
Han, Xue [4 ]
Zhao, Xia [4 ]
Wang, Yi [3 ]
Wu, Gaojun [1 ,2 ]
Luo, Wu [1 ,2 ,3 ]
Liang, Guang [1 ,2 ,3 ,4 ]
Shan, Peiren [1 ,2 ]
机构
[1] Wenzhou Med Univ, Affiliated Hosp 1, Dept Cardiol, Wenzhou, Zhejiang, Peoples R China
[2] Wenzhou Med Univ, Affiliated Hosp 1, Key Lab Cardiovasc Dis Wenzhou, Wenzhou, Zhejiang, Peoples R China
[3] Wenzhou Med Univ, Sch Pharmaceut Sci, Chem Biol Res Ctr, Wenzhou, Zhejiang, Peoples R China
[4] Hangzhou Med Coll, Sch Pharmaceut Sci, Hangzhou, Zhejiang, Peoples R China
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2023年 / 1869卷 / 06期
关键词
Diabetic cardiomyopathy; Dectin-1; Inflammation; Macrophages; Nuclear factor-& kappa; B; BETA-GLUCAN RECEPTOR; INNATE IMMUNE; ACTIVATION; RECOGNITION; MECHANISMS; INDUCTION; TOLERANCE; MODELS; IMPACT; CELLS;
D O I
10.1016/j.bbadis.2023.166710
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiovascular diseases are the primary cause of mortality in patients with diabetes and obesity. Hyperglycemia and hyperlipidemia in diabetes alters cardiac function, which is associated with broader cellular processes such as aberrant inflammatory signaling. Recent studies have shown that a pattern recognition receptor called Dectin1, expressed on macrophages, mediates pro-inflammatory responses in innate immunity. In the present study, we examined the role of Dectin-1 in the pathogenesis of diabetic cardiomyopathy. We observed increased Dectin-1 expression in heart tissues of diabetic mice and localized the source to macrophages. We then investigated the cardiac function in Dectin-1-deficient mice with STZ-induced type 1 diabetes and high-fat-diet-induced type 2 diabetes. Our results show that Dectin-1 deficient mice are protected against diabetes-induced cardiac dysfunction, cardiomyocyte hypertrophy, tissue fibrosis, and inflammation. Mechanistically, our studies show that Dectin-1 is important for cell activation and induction of inflammatory cytokines in high-concentration glucose and palmitate acid (HG + PA)-challenged macrophages. Deficiency of Dectin-1 generate fewer paracrine inflammatory factors capable of causing cardiomyocyte hypertrophy and fibrotic responses in cardiac fibroblasts. In conclusion, this study provides evidence that Dectin-1 mediates diabetes-induced cardiomyopathy through regulating inflammation. Dectin-1 may be a potential target to combat diabetic cardiomyopathy.
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页数:13
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