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

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 signif...

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Detalles Bibliográficos
Autores principales: Liu, Hong, Huang, Yimao, Zhao, Yang, Kang, Gyeoung-Jin, Feng, Feng, Wang, Xiaodan, Liu, Man, Shi, Guangbin, Revelo, Xavier, Bernlohr, David, Dudley, Samuel C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Original Research - Preclinical
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9998610/
https://www.ncbi.nlm.nih.gov/pubmed/36908663
http://dx.doi.org/10.1016/j.jacbts.2022.08.003
Descripción
Sumario: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.

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