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摘要: 慢性心力衰竭(chronic heart failure,CHF)是各类心血管疾病的终末期阶段。CHF的治疗方案近年虽不断完善,但仍有较高的死亡率与住院率,给患者及家庭带来了巨大的医疗负担。CHF的具体机制目前尚未完全明确,寻找CHF发生发展的病理生理机制及相关治疗靶点迫在眉睫。已知炎症在CHF的发展中起着重要作用,而NLRP3炎性小体可能在其中起重要的桥梁与驱动作用。但在CHF的发展过程中,不同病理条件下的NLRP3炎性小体激活机制有所差异。并且激活后的NLRP3炎性小体对不同的细胞可产生不同的病理作用。了解NLRP3炎性小体的激活机制及其在CHF中的作用或许可为CHF提供新的治疗靶点。本文就NLRP3炎性小体在CHF发生发展中的作用、机制及相关治疗作一综述。Abstract: Chronic heart failure(CHF) is the terminal stage of cardiovascular disease. Although the treatment of CHF has been continuously improved in recent years, there are still high mortality and hospitalization rates, which bring huge medical burden to patients and families. The specific mechanism of CHF has not yet been fully clarified. It is urgent to find the pathophysiological mechanism and related therapeutic targets of CHF. It is known that inflammation plays an important role in the development of CHF, and NLRP3 inflammasome may play an important bridge and driving role. However, in the development of CHF, the mechanism of NLRP3 inflammasome activation is different under different pathological conditions. And the activated NLRP3 inflammasome can have different pathological effects on different cells. and targeted therapy for NLRP3 inflammasome has also made progress in recent years. In this paper, we review the role, mechanism and related treatment of NLRP3 inflammasome in the development of CHF.
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Key words:
- inflammation /
- NLRP3 /
- inflammasome /
- chronic heart failure /
- mechanism
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