Inflammation, Immunity, and Infection in Atherothrombosis: JACC Review Topic of the Week.

Inflammation, Immunity, and Infection in Atherothrombosis: JACC Review Topic of the Week.
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DOI:
10.1016/j.jacc.2018.08.1043
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发表时间:
2018-10-23
影响因子:
24
通讯作者:
Amar S
Amar S
中科院分区:
医学1区
文献类型:
--
作者:
Libby P;Loscalzo J;Ridker PM;Farkouh ME;Hsue PY;Fuster V;Hasan AA;Amar S

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对人类和实验性动脉粥样硬化的观察,生物标志物研究,以及现在的大规模临床试验支持这种疾病中免疫和炎症途径的运作。引发与动脉粥样硬化形成和病变并发症有关的先天性和适应性免疫反应的因素包括传统的风险因素,如天然和修饰的低密度脂蛋白(LDL)的蛋白质和脂质成分、血管紧张素II、吸烟、内脏脂肪组织和代谢异常。内源性微生物组的感染过程和产物也可能通过引发增强疾病表达的局部和全身反应来直接或间接调节动脉粥样硬化及其并发症。抗生素试验并没有减少心血管事件的复发,疫苗接种策略也没有实现临床转化。然而,抗炎干预措施,如抗细胞因子治疗和秋水仙碱已开始证明在这方面的疗效。因此,炎症和免疫机制可以将传统和新兴的危险因素与动脉粥样硬化联系起来,并提供新的干预途径。免疫和炎症途径有助于动脉粥样硬化及其临床并发症。刺激动脉粥样硬化形成和病变并发症中涉及的先天性和适应性免疫应答的因素包括传统危险因素的方面。感染也可能直接或间接地通过引发增强疾病表达的局部和全身反应来调节动脉粥样硬化及其并发症。尽管抗生素试验没有减少心血管事件的复发,疫苗接种策略也没有实现临床转化,但抗炎干预措施已经开始显示出疗效。因此,炎症和免疫机制可以将传统和新兴的危险因素与动脉粥样硬化联系起来,并提供新的干预途径。
Observations on human and experimental atherosclerosis, biomarker studies, and now a large-scale clinical trial support the operation of immune and inflammatory pathways in this disease. The factors that incite innate and adaptive immune responses implicated in atherogenesis and in lesion complication include traditional risk factors such as protein and lipid components of native and modified low-density lipoprotein (LDL), angiotensin II, smoking, visceral adipose tissue, and dysmetabolism. Infectious processes and products of the endogenous microbiome might also modulate atherosclerosis and its complications either directly or indirectly by eliciting local and systemic responses that potentiate disease expression. Trials with antibiotics have not reduced recurrent cardiovascular events, nor have vaccination strategies yet achieved clinical translation. Yet, anti-inflammatory interventions such as anti-cytokine therapy and colchicine have begun to demonstrate efficacy in this regard. Thus, inflammatory and immune mechanisms can link traditional and emerging risk factors to atherosclerosis, and offer novel avenues for intervention. Immune and inflammatory pathways contribute to atherogenesis and its clinical complications. The factors that incite innate and adaptive immune responses implicated in atherogenesis and in lesion complication include aspects of traditional risk factors. Infections might also modulate atherosclerosis and its complications either directly or indirectly by eliciting local and systemic responses that potentiate disease expression. Although trials with antibiotics have not reduced recurrent cardiovascular events, nor have vaccination strategies yet achieved clinical translation, anti-inflammatory interventions have begun to demonstrate efficacy. Thus, inflammatory and immune mechanisms can link traditional and emerging risk factors to atherosclerosis, and offer novel avenues for intervention.
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