Macrophage–fibroblast interactions have a central role in cardiac fibrosis. In response to left ventricular pressure overload, CCR2+ cardiac macrophages acquire a fibrogenic phenotype, secreting IL-1β and promoting the activation of a FAP+ POSTN+ fibroblast subpopulation through the transcription factor MEOX1. Macrophage-derived fibroblast-activating cytokines (such as IL-1β), growth factors and matricellular proteins contribute to the pathogenesis of heart failure.
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Acknowledgements
The author’s laboratory is supported by NIH grants R01 HL76246, R01 HL85440 and R01 HL149407, and by the US Department of Defense grant PR211352.
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Frangogiannis, N.G. Targeting macrophage–fibroblast interactions in the failing heart. Nat Rev Cardiol (2024). https://doi.org/10.1038/s41569-024-01112-z
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DOI: https://doi.org/10.1038/s41569-024-01112-z
