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

Autor:	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 Jr; Division of Cardiology, Department of Medicine, the Lillehei Heart Institute, University of Minnesota, Minneapolis, Minnesota, USA.
Jazyk:	angličtina
Zdroj:	JACC. Basic to translational science [JACC Basic Transl Sci] 2022 Nov 30; Vol. 8 (2), pp. 174-185. Date of Electronic Publication: 2022 Nov 30 (Print Publication: 2023).
DOI:	10.1016/j.jacbts.2022.08.003
Abstrakt:	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. Competing Interests: This project was supported by National Institutes of Health grants R01 HL104025 (Dr Dudley) and R01 HL106592 (Dr Dudley). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. (© 2023 The Authors.)
Databáze:	MEDLINE
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