INFLAMMATORY MEDIATORS LEAD TO CAROTID PLAQUE INSTABILITY AND RUPTURE

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这个项目的目标是填补我们在颈动脉斑块不稳定和破裂过程中的主要知识空白。颈动脉疾病是脑血管疾病的重要原因，仍然是一个主要的医疗保健问题，在美国每年至少导致20万例中风。在这些案例中，几乎有一半在一年内死亡。这些事件的机制是通过颈动脉斑块不稳定、破裂和动脉粥样硬化栓塞术。 越来越多的证据表明，颈动脉狭窄程度以外的其他因素也参与了缺血性中风的风险。根据患者的临床表现，颈动脉粥样硬化斑块传统上被描述为“稳定”或“不稳定”。斑块稳定性与不太可能发生的动脉粥样硬化栓塞化事件有关，而“不稳定”或斑块脆弱性导致斑块破裂和眼或大脑半球事件的可能性更大。尽管其中一些斑块的差异可以通过超声波来识别，但没有好的生化标志物存在。此外，导致稳定的颈动脉斑块向不稳定的斑块转化的发病机制尚不清楚。我们已经在该地区的多家医院获得了IRB的批准，以研究炎症介质在颈动脉粥样硬化斑块从稳定斑块向脆弱和不稳定斑块发展过程中所起的作用。此外，我们的目标是研究稳定和不稳定颈动脉斑块之间的关键分子差异。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The goal of this project is to fill major gaps in our knowledge regarding the process of carotid plaque instability and rupture. Carotid artery disease is an important cause of cerebrovascular disease and continues to be a major health care problem, contributing to at least 200,000 cases of stroke each year the United States. In almost half of these cases, death follows within a year. The mechanism for these events is via carotid plaque instability, rupture, and atheroembolization. Increasing evidence suggests that factors other than the degree of carotid stenosis are involved in the risk of ischemic stroke. Carotid atherosclerotic plaques have traditionally been characterized as "stable" or "unstable" by the clinical presentation of the patient. Plaque stability relates to the unlikely event of atheroembolization, while "instability" or plaque vulnerability, invokes the greater potential for plaque rupture and ocular or cerebral hemispheric events. Even though some of these plaque differences can be appreciated sonographically, no good biochemical markers exist. Furthermore, the pathogenesis which leads a stable carotid plaque towards an unstable one is poorly understood. We have obtained IRB approval at various hospitals in the area to study the role that inflammatory mediators play in carotid atherosclerotic plaque progression from a stable to a vulnerable, unstable plaque. Furthermore, we aim to study the key molecular differences between stable and unstable carotid plaques.