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Targeting macrophage–fibroblast interactions in the failing heart
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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Targeting macrophage–fibroblast interactions in the failing heart