ReviewFrontiers in cell and developmental biology2026
Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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 factor (HIF) signaling, thereby reshaping intercellular communication among non-myocytes. This mini-review presents the latest evidence on hypoxia-driven fibrosis through three processes: (i) fibroblast activation and myofibroblast differentiation, (ii) macrophage polarization and paracrine effects, and (iii) endothelial-to-mesenchymal transition (EndMT). Recent single-cell transcriptomics studies have revealed fibroblast/immune cell heterogeneity post-injury, while metabolic shifts (e.g., glycolytic reprogramming, lactate-histone lactylation, and glutamine persistence) link hypoxia to the epigenetic regulation of fibrosis. Novel therapies, including lactate-scavenging biomaterials, eNAMPT neutralization, and timed metalloproteinase inhibition, show promise in targeting these pathways. A deeper understanding of hypoxia-mediated crosstalk may lead to the development of strategies to mitigate maladaptive fibrosis while preserving reparative scarring following MI.
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