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

Liu, Hong; Huang, Yimao; Zhao, Yang; Kang, Gyeoung-Jin; Feng, Feng; Wang, Xiaodan; Liu, Man; Shi, Guangbin; Revelo, Xavier; Bernlohr, David; Dudley, Samuel C

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

Liu, Hong; Huang, Yimao; Zhao, Yang; Kang, Gyeoung-Jin; Feng, Feng; Wang, Xiaodan; Liu, Man; Shi, Guangbin; Revelo, Xavier; Bernlohr, David; Dudley, Samuel C.

Afiliação

Liu H; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Huang Y; Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota, USA.
Zhao Y; Division of Cardiology, Lanzhou University Second Hospital, Lanzhou University, Lanzhou, Gansu, China.
Kang GJ; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Feng F; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Wang X; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Liu M; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Shi G; Division of Cardiology, Cardiovascular Research Center, Rhode Island Hospital, Warren Alpert Medical School of Brown University, Providence, Rhode Island, USA.
Revelo X; Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, Minnesota, USA.
Bernlohr D; Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota, USA.
Dudley SC; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.

JACC Basic Transl Sci ; 8(2): 174-185, 2023 Feb.

Article em En | MEDLINE | ID: mdl-36908663

ABSTRACT

ABSTRACT

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)-1ß levels, and proinflammatory cardiac macrophage accumulation. DD was significantly ameliorated by suppressing IL-1ß signaling or depleting macrophages. Mice with macrophages unable to adopt a proinflammatory phenotype were low in cardiac IL-1ß levels and were resistant to HFD-induced DD. IL-1ß 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-1ß and mitoROS production.

Palavras-chave

CCR2, C-C motif chemokine receptor 2; CM, cardiomyocyte; DD, diastolic dysfunction; DM, diabetes mellitus; EF, ejection fraction; FABP4, fatty acid binding protein 4; HF, heart failure; HFD, high-fat diet; HFpEF; HFpEF, heart failure with preserved ejection fraction; IL, interleukin; IL-1ß; IL1RA, interleukin 1 receptor antagonist; KO, knockout; MCP, monocyte chemoattractant protein; MyBP-C, myosin binding protein C; TGF, transforming growth factor; TNF, tumor necrosis factor; Timd4, T cell immunoglobulin and mucin domain containing 4; WT, wild-type; diabetes; diastolic dysfunction; inflammation; macrophage; mitoROS, mitochondrial reactive oxygen species; mitochondria

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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Ano de publicação: 2023 Tipo de documento: Article

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PubMed Links

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Texto completo: 1 Base de dados: MEDLINE Tipo de estudo: Risk_factors_studies Idioma: En Ano de publicação: 2023 Tipo de documento: Article