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

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

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

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)-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.

Original languageEnglish (US)
Pages (from-to)174-185
Number of pages12
JournalJACC: Basic to Translational Science
Volume8
Issue number2
DOIs
StatePublished - Feb 2023

Bibliographical note

Publisher Copyright:
© 2023 The Authors

Keywords

  • HFpEF
  • IL-1β
  • diabetes
  • diastolic dysfunction
  • inflammation
  • macrophage
  • mitochondria

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