Inflammatory Macrophage Interleukin-1b Mediates High-Fat Diet-Induced Heart Failure With Preserved Ejection Fraction

被引：32
作者：
Liu, Hong [1 ]
Huang, Yimao [2 ]
Zhao, Yang [3 ]
Kang, Gyeoung-Jin [1 ]
Feng, Feng [1 ]
Wang, Xiaodan [1 ]
Liu, Man [1 ]
Shi, Guangbin [4 ]
Revelo, Xavier [5 ]
Bernlohr, David [2 ]
Dudley, Samuel C. [1 ,6 ]
机构：
[1] Univ Minnesota, Lillehei Heart Inst, Dept Med, Div Cardiol, Minneapolis, MN USA
[2] Univ Minnesota, Dept Biochem Mol Biol & Biophys, Minneapolis, MN USA
[3] Lanzhou Univ, Hosp 2, Div Cardiol, Lanzhou, Gansu, Peoples R China
[4] Brown Univ, Rhode Isl Hosp,Warren Alpert Med Sch, Cardiovasc Res Ctr, Div Cardiol, Providence, RI USA
[5] Univ Minnesota, Dept Integrat Biol & Physiol, Minneapolis, MN USA
[6] Univ Minnesota, Div Cardiol, VCRC 286 MMC 508,420 Delaware St,SE, Minneapolis, MN 55455 USA
来源：
JACC-BASIC TO TRANSLATIONAL SCIENCE | 2023年 / 8卷 / 02期
基金：
美国国家卫生研究院;
关键词：
diabetes; diastolic dysfunction; HFpEF; IL-1b; inflammation; macrophage; mitochondria; DIASTOLIC DYSFUNCTION; DIABETES-MELLITUS; CARDIAC FIBROSIS; ACTIVATION; IL-1-BETA; INDUCTION; DEPLETION; INJURY; DEATH;
D O I：
10.1016/j.jacbts.2022.08.003
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Diabetes mellitus (DM) is a main risk factor for diastolic dysfunction (DD) and heart failure with preserved ejection fraction. High-fat diet (HFD) mice presented with diabetes mellitus, DD, higher cardiac interleukin (IL)-1β levels, and proinflammatory cardiac macrophage accumulation. DD was significantly ameliorated by suppressing IL-1β signaling or depleting macrophages. Mice with macrophages unable to adopt a proinflammatory phenotype were low in cardiac IL-1β levels and were resistant to HFD-induced DD. IL-1β enhanced mitochondrial reactive oxygen species (mitoROS) in cardiomyocytes, and scavenging mitoROS improved HFD-induced DD. In conclusion, macrophage-mediated inflammation contributed to HFD-associated DD through IL-1β and mitoROS production. © 2023 The Authors
引用
收藏
页码：174 / 185
页数：12
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