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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques
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The role of damage- and pathogen-associated molecular patterns in inflammation-mediated vulnerability of atherosclerotic plaques

机译：损伤和病原体相关分子模式在动脉粥样硬化斑块的炎症介导的脆弱性中的作用

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摘要

Atherosclerosis is a chronic inflammatory disease resulting in the formation of the atherosclerotic plaque. Plaque formation starts with the inflammation in fatty streaks and progresses through atheroma, atheromatous plaque, and fibroatheroma leading to development of stable plaque. Hypercholesterolemia, dyslipidemia, and hyperglycemia are the risk factors for atherosclerosis. Inflammation, infection with viruses and bacteria, and dysregulation in the endothelial and vascular smooth muscle cells leads to advanced plaque formation. Death of the cells in the intima due to inflammation results in secretion of damage-associated molecular patterns (DAMPs) such as high mobility group box 1 (HMGB1), receptor for advanced glycation end products (RAGE), alarmins (S100A8, S100A9, S100A12, and oxidized low-density lipoproteins), and infection with pathogens leads to secretion of pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharides, lipoteichoic acids, and peptidoglycans. DAMPs and PAMPs further activate the inflammatory surface receptors such as TREM-1 and toll-like receptors and downstream signaling kinases and transcription factors leading to increased secretion of pro-inflammatory cytokines such as tumor necrosis factor α, interleukin (IL)-1β, IL-6, and interferon-γ and matrix metalloproteinases (MMPs). These mediators and cytokines along with MMPs render the plaque vulnerable for rupture leading to ischemic events. In this review, we have discussed the role of DAMPs and PAMPs in association with inflammation-mediated plaque vulnerability.
机译：动脉粥样硬化是一种慢性炎症疾病，导致形成动脉粥样硬化斑块。斑块形成从脂肪条纹中的炎症开始，通过运动粥样硬化，斑块斑块和纤维斑疹进展，导致稳定斑块的发展。高胆固醇血症，血脂血症和高血糖是动脉粥样硬化的危险因素。炎症，病毒和细菌感染，内皮和血管平滑肌细胞中的失调导致先进的斑块形成。由于炎症引起的内膜中的细胞死亡导致损伤相关的分子模式（潮湿），例如高迁移率组箱1（HMGB1），用于先进的糖化末端产物（RAGE），警报（S100A8，S100A9，S100A12的受体和氧化的低密度脂蛋白），以及病原体的感染导致分泌病原体相关的分子模式（PAMP），例如脂多糖，脂素内酸和肽聚糖。潮湿和纸浆进一步激活炎症表面受体，例如Trem-1和损伤的受体和下游信号调节和转录因子，导致促炎细胞因子的分泌增加，例如肿瘤坏死因子α，白细胞介素（IL）-1β，IL -6，和干扰素-γ和基质金属蛋白酶（MMPS）。这些介质和细胞因子以及MMPS使斑块易受破裂的斑块导致缺血事件。在本次审查中，我们讨论了潮湿和纸浆与炎症介导的斑块脆弱性的作用。

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