Autonomous driving paper index
Hypoxia-driven crosstalk among cardiac fibroblasts, macrophages, and endothelial cells in cardiac fibrosis
One-line summary
Cardiac fibrosis, a hallmark of adverse remodeling following myocardial infarction (MI), markedly contributes to progressive heart failure.
Engineering notes
Key topics: autonomous driving. See the paper for implementation details and experimental results.
Chinese explanation / 中文解读
中文解读待补充：本站会优先为端到端自动驾驶、BEV感知、3D目标检测、轨迹预测、路径规划、LiDAR感知等高价值论文补充中文说明。
Original 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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