内皮剪切应力指标与冠状动脉侵蚀罪魁祸首的促炎途径有关

IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Mona E. Ahmed MD, PhD , David M. Leistner MD , Diaa Hakim MD, PhD , Youssef Abdelwahed MD , Ahmet U. Coskun PhD , Charles Maynard PhD , Claudio Seppelt MD , Gregor Nelles MD , Denitsa Meteva MD , Nicholas V. Cefalo BS , Peter Libby MD , Ulf Landmesser MD , Peter H. Stone MD
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引用次数: 0

摘要

低内皮剪切应力(ESS)和相关的不良生物力学特征会刺激炎症,导致动脉粥样硬化,并容易造成冠状动脉斑块破坏。然而,与血流相关的不良血流动力学与斑块侵蚀所涉及的炎症介质之间的机理联系仍然鲜有探索。我们研究了急性冠状动脉综合征患者的高风险ESS指标与冠状动脉斑块侵蚀的罪魁祸首病变原炎/致动脉粥样硬化细胞和细胞因子/凝血因子之间的关系。在侵蚀斑块中,低ESS、高ESS梯度和斑块地形坡度的陡度与局部T细胞和亚群(CD4+、CD8+、自然杀伤T细胞)以及炎症介质(白细胞介素[IL]-6、巨噬细胞炎症蛋白-1β、IL-1β、IL-2)数量的增加有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endothelial Shear Stress Metrics Associate With Proinflammatory Pathways at the Culprit Site of Coronary Erosion
Low endothelial shear stress (ESS) and associated adverse biomechanical features stimulate inflammation, contribute to atherogenesis, and predispose to coronary plaque disruption. The mechanistic links between adverse flow-related hemodynamics and inflammatory mediators implicated in plaque erosion, however, remain little explored. We investigated the relationship of high-risk ESS metrics to culprit lesion proinflammatory/proatherogenic cells and cytokines/chemokines implicated in coronary plaque erosion in patients with acute coronary syndromes. In eroded plaques, low ESS, high ESS gradient, and steepness of plaque topographical slope associated with increased numbers of local T cells and subsets (CD4+, CD8+, natural killer T cells) as well as inflammatory mediators (interleukin [IL]-6, macrophage inflammatory protein-1β, IL-1β, IL-2).
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来源期刊
JACC: Basic to Translational Science
JACC: Basic to Translational Science CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
14.20
自引率
1.00%
发文量
161
审稿时长
16 weeks
期刊介绍: JACC: Basic to Translational Science is an open access journal that is part of the renowned Journal of the American College of Cardiology (JACC). It focuses on advancing the field of Translational Cardiovascular Medicine and aims to accelerate the translation of new scientific discoveries into therapies that improve outcomes for patients with or at risk for Cardiovascular Disease. The journal covers thematic areas such as pre-clinical research, clinical trials, personalized medicine, novel drugs, devices, and biologics, proteomics, genomics, and metabolomics, as well as early phase clinical trial methodology.
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