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  • Neutrophil Extracellular Traps (NETs) as drivers of . . .
    Macrophages ingest cholesterol and become foam cells, triggering sustained inflammation and immune activation This leads to plaque formation with immune and smooth muscle cell infiltration, narrowing the arterial lumen
  • Macrophage polarization and metabolism in atherosclerosis
    In this complex scenario of atherosclerosis, macrophages participate in the whole process, including the initiation, growth and eventually rupture and wound healing stages of artery plaque
  • Macrophage-based pathogenesis and theranostics of . . .
    Vulnerable plaques, which are high-risk features of atherosclerosis, constitute critical elements in the disease's progression due to their formation and rupture Macrophages and macrophage-derived foam cells are pivotal in inducing vulnerability within atherosclerotic plaques
  • Macrophage DNases Limit Neutrophil Extracellular Trap . . .
    Macrophages play a key role in clearing NETs from tissues Endoplasmic reticulum stress suppresses macrophage DNase secretion, leading to NET accumulation in atherosclerotic plaques, which triggers efferocytosis impairment and plaque progression
  • Frontiers | Interactions between neutrophil extracellular traps . . .
    In AS, NETs and macrophages establish a self-sustaining vicious cycle—initiated by lipid infiltration, perpetuated through foam cell formation and inflammatory amplification, and exacerbated by impaired repair processes—which collectively drive plaque onset, progression, and eventual rupture
  • Macrophage-based pathogenesis and theranostics of . . .
    This review aims to summarize the main pathological processes, in vivo mouse models, and macrophage-based insights into atherosclerotic vulnerable plaques Additionally, it examines current strategies targeting macrophages or foam cells for the diagnosis and treatment of vulnerable plaques
  • Macrophage polarization and metabolism in atherosclerosis
    During the development of atherosclerosis, abundant apoptotic macrophages or neutrophil extracellular traps (NETs) within plaques cannot be removed by surrounding macrophages because of
  • Human monocyte-derived macrophages: Pathogenetic role in . . .
    The present study is the first to investigate the pathophysiological role of MDMs in coronary plaque destabilization and it puts in evidence a close relationship between the most pro-thrombotic, pro-inflammatory and pro-oxidant macrophage subpopulation and plaque rupture
  • Neutrophil extracellular traps: a catalyst for atherosclerosis
    Continuous release of NETs in response to external stimuli leads to activation of surrounding platelets and monocytes macrophages, resulting in damage to endothelial cells (EC) and vascular smooth muscle cells (VSMC)





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