急性心肌梗死和中风均为高致死致残类疾病，其潜在机制均为易损斑块。上述病理环节中炎症和组织修复是决定斑块易损性的重要因素。本项目将着眼于揭示炎症和组织修复是如何影响斑块进展的具体机制，从而为今后的早期诊断和有效干预提供新的靶点和策略。为此本联合项目将进行以下工作：1、揭示调节人中晚期动脉粥样硬化斑块炎症和组织修复的关键因素；2、联合分析模型动物、人颈动脉血管组织以及血清标本揭示相关的免疫机制；3、发现并验证反应血管重构和修复进程的临床生物标志物。为了达成上述目标，联合项目双方将动员各自的技术力量、交流各自特有的动物模型、完善并进一步强化现存于马尔默和上海的组织标本库以及临床队列研究数据。

Acute myocardial infarction and stroke are common diseases, which causes disablement and mortality. The underlying mechanisms are often a vulnerable atherosclerotic plaque. Inflammation and tissue repair in the atherosclerotic lesion are important players in these different conditions. This project will expand the understanding on how mechanisms for inflammation and tissue repair in the plaque influence the atherosclerotic process. This wil provide new therapeutic targets and strategies for the diagnosis and treatment of cardiovascular disease. While there has been considerable focus on inflammation in destabilization of atherosclerotic lesions there has been less focus on how inflammation and other factors.regulate tissue repair in the atherosclerotic plaque. To address this issue present new joint Swedish-Chinese project aims to: (1) characterize the factors that regulate inflammation and repair responses in advanced human atherosclerotic plaques, (2) use a combination of experimental animal models, expression analysis in human vascular tissue and clinical biomarkers to characterize protective immune pathways of relevance for cardiovascular disease in humans and (3) identify and validate clinical biomarkers for cardiovascular disease risk reflecting vascular remodeling and repair processes. In order to reach these aims we use unique and complementary expertize, experimental models, biobanks and clinical cohorts available in Malmö and Shanghai.