背景:动脉粥样硬化,传统上被认为是脂质相关疾病,现在被认为是一种具有重大全球健康影响的慢性炎症。
目的:这篇综述旨在深入研究免疫细胞之间的复杂相互作用,细胞因子,和动脉粥样硬化中的炎症级联反应,阐明这些元素如何影响疾病的开始和进展。
方法:这篇综述借鉴了最近的临床研究来阐明关键免疫细胞的作用。巨噬细胞,T细胞,内皮细胞,和克隆造血在动脉粥样硬化的发展。它专注于这些细胞和过程如何促进疾病的发生和发展,特别是通过炎症驱动的过程,导致斑块形成和稳定。巨噬细胞摄取氧化低密度脂蛋白(oxLDL),部分转化为高密度脂蛋白(HDL)或积累为脂滴,形成对斑块稳定性至关重要的泡沫细胞。此外,巨噬细胞在斑块内表现出不同的表型,以促炎类型为主,其他专门从事破裂部位的碎片清除。CD4+T和CD8+T细胞参与这些过程促进炎性巨噬细胞状态,抑制血管平滑肌细胞增殖,并增强斑块的不稳定性。
结果:巨噬细胞的细微差别作用,T细胞,并探索动脉粥样硬化微环境中的相关免疫细胞,揭示了对引发炎症的细胞和分子途径的见解。这篇综述还讨论了成像和生物标志物技术的最新进展,这些进展增强了我们对疾病进展的理解。此外,它指出了当前治疗的局限性,并强调了新兴的抗炎策略的潜力,包括p38MAPK等药物的临床试验,肿瘤坏死因子α(TNF-α),和IL-1β,他们的初步结果,和canakinumab的有希望的效果,秋水仙碱,和IL-6R拮抗剂。
结论:这篇综述探讨了尖端的抗炎干预措施,它们在预防和缓解动脉粥样硬化方面的潜在功效,以及纳米技术在更有效和安全地提供药物方面的作用。
BACKGROUND: Atherosclerosis, traditionally considered a lipid-related disease, is now understood as a chronic inflammatory condition with significant global health implications.
OBJECTIVE: This review aims to delve into the complex interactions among immune cells, cytokines, and the inflammatory cascade in atherosclerosis, shedding light on how these elements influence both the initiation and progression of the disease.
METHODS: This review draws on recent clinical research to elucidate the roles of key immune cells, macrophages, T cells, endothelial cells, and clonal hematopoiesis in atherosclerosis development. It focuses on how these cells and process contribute to disease initiation and progression, particularly through inflammation-driven processes that lead to plaque formation and stabilization. Macrophages ingest oxidized low-density lipoprotein (oxLDL), which partially converts to high-density lipoprotein (HDL) or accumulates as lipid droplets, forming foam cells crucial for plaque stability. Additionally, macrophages exhibit diverse phenotypes within plaques, with pro-inflammatory types predominating and others specializing in debris clearance at rupture sites. The involvement of CD4+ T and CD8+ T cells in these processes promotes inflammatory macrophage states, suppresses vascular smooth muscle cell proliferation, and enhances plaque instability.
RESULTS: The nuanced roles of macrophages, T cells, and the related immune cells within the atherosclerotic microenvironment are explored, revealing insights into the cellular and molecular pathways that fuel inflammation. This review also addresses recent advancements in imaging and biomarker technology that enhance our understanding of disease progression. Moreover, it points out the limitations of current treatment and highlights the potential of emerging anti-inflammatory strategies, including clinical trials for agents such as p38MAPK, tumor necrosis factor α (TNF-α), and IL-1β, their preliminary outcomes, and the promising effects of canakinumab, colchicine, and IL-6R antagonists.
CONCLUSIONS: This review explores cutting-edge anti-inflammatory interventions, their potential efficacy in preventing and alleviating atherosclerosis, and the role of nanotechnology in delivering drugs more effectively and safely.