Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis
Cardiac fibrosis, a hallmark of adverse remodeling following myocardial infarction (MI), markedly contributes to progressive heart failure. Severe tissue hypoxia within the ischemic heart activates hypoxia-inducible fact
This paper presents the latest evidence on hypoxia-driven fibrosis in cardiac fibrosis, a hallmark of adverse remodeling following myocardial infarction (MI). Severe tissue hypoxia within the ischemic heart activates hypoxia-inducible factor (HIF) signaling, reshaping intercellular communication among non-myocytes. Recent studies have revealed fibroblast/immune cell heterogeneity post-injury and metabolic shifts linking hypoxia to epigenetic regulation of fibrosis. Novel therapies targeting these pathways show promise in mitigating maladaptive fibrosis while preserving reparative scarring following MI. The authors highlight the importance of understanding hypoxia-mediated crosstalk in cardiac fibrosis, which may lead to the development of new strategies to address this condition.