NLRP3炎症小体与心血管疾病

发布时间：2018-07-15 10:41

【摘要】：炎症小体是一类多蛋白复合物,主要由识别炎症的胞浆型模式识别受体、衍接蛋白和效应蛋白三部分组成。炎症小体组装激活可以自我切割生成活性形式的caspase-1,并进一步促进白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)等炎症因子的成熟和释放,引起炎症反应。此外炎症小体激活可介导caspase-1依赖的细胞焦亡,从而促进炎症反应的扩散。炎症小体根据识别信号的模式识别受体命名,其中NLRP3炎症小体是目前研究最多了解相对最清楚的炎症小体。最新研究表明心血管疾病的多种危险因素如脂代谢紊乱、高血压及肾脏疾病、高同型半胱氨酸血症、肥胖、糖尿病及代谢综合征等均可以激活NLRP3炎症小体,促进炎性介质IL-1β和IL-18等的表达、释放,促进动脉粥样硬化发生发展,并影响动脉粥样斑块的稳定性,提示其在心血管疾病发病机制中的重要作用。干预NLRP3炎症小体的生成、活化,可望为心血管疾病的防治提供新的思路。
[Abstract]:Inflammatory body is a kind of polyprotein complex, which consists of three parts: cytosolic pattern recognition receptor, derivative protein and effector protein. Inflammatory body assembly can activate caspase-1 in the form of caspase-1, and further promote the maturation and release of inflammatory factors such as interleukin-1 尾 (IL-1 尾) and interleukin-18 (IL-18), resulting in inflammatory reaction. In addition, the activation of inflammatory corpuscles can mediate caspase-1 dependent cell pyrolysis, thus promoting the spread of inflammatory response. The inflammatory corpuscles are named according to the pattern recognition receptors of recognition signals, and NLRP3 inflammatory corpuscles are the most well known inflammatory corpuscles. Recent studies have shown that various risk factors for cardiovascular disease, such as dyslipidemia, hypertension and kidney disease, hyperhomocysteinemia, obesity, diabetes and metabolic syndrome, can activate NLRP3 inflammatory corpuscles. It can promote the expression and release of IL-1 尾 and IL-18, promote the development of atherosclerosis and affect the stability of atherosclerotic plaques, which indicates the important role of IL-1 尾 and IL-18 in the pathogenesis of cardiovascular disease. Intervention in the formation and activation of NLRP3 inflammatory corpuscles is expected to provide new ideas for the prevention and treatment of cardiovascular diseases.
【作者单位】：中山大学中山医学院病理生理学教研室;中山大学中山医学院心血管研究群体;
【基金】：国家自然科学基金(81370371,81570394) 广东省自然科学基金(2014A030313066)
【分类号】：R54

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