INFLAMMATORY MEDIATORS LEAD TO CAROTID PLAQUE INSTABILITY AND RUPTURE

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 这个项目的目标是填补我们对颈动脉斑块不稳定和破裂过程的认识的主要空白。 颈动脉疾病是脑血管疾病的一个重要原因，并且仍然是一个主要的卫生保健问题，在美国每年至少有20万例中风病例。 在这些病例中，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。 越来越多的证据表明，颈动脉狭窄程度以外的因素也参与了缺血性卒中的风险。 颈动脉粥样硬化斑块传统上根据患者的临床表现被表征为“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有关，而“不稳定性”或斑块脆弱性则更有可能引起斑块破裂和眼或大脑半球事件。 尽管超声检查可以发现其中一些斑块差异，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斑块的发病机制知之甚少。 我们已获得IRB批准，在该地区的多家医院研究炎症介质在颈动脉粥样硬化斑块从稳定斑块进展到脆弱、不稳定斑块中的作用。 此外，我们的目标是研究稳定和不稳定的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.