Toll样受体在钙化性主动脉瓣疾病中的研究进展

Research progress of Toll-like receptors in calcified aortic valve disease

钙化性主动脉瓣疾病(calcified aortic valve disease,CAVD)既往被认为是由衰老相关的退行性病变和被动的钙盐沉积所导致,近年来发现CAVD实际是一个主动的病理过程,其发病机制尚未阐明。在CAVD的发展过程中,先天免疫反应和适应性免疫反应均被激活,越来越多的证据表明,炎症在疾病的起始和发展阶段起着核心作用,其中Toll样受体(Toll-like receptors,TLRs)的功能尤其重要。TLRs通过识别病原体和组织损伤后释放的宿主衍生分子,充当先天免疫系统的哨兵,在控制感染和维持组织稳态中发挥关键作用。本文通过概述目前关于TLRs信号传导与CAVD发病机制中炎症和钙化重塑之间的关系,以期为CAVD的治疗提供新的靶点和策略。

Calcified aortic valve disease(CAVD)was believed to be caused by aging-associated degenerative changes and passive calcium deposition.In recent years,it has been found that CAVD is an active pathological process,but the possible pathogenesis of CAVD has not been elucidated.During the development of CAVD,both innate and adaptive immune responses are activated,and increasing evidence suggests that inflammation plays a central role in the initiation and progression of the disease,in which the function of Toll-like receptors(TLRs)is particularly important.TLRs play a crucial role in controlling infection and maintaining tissue homeostasis by identifying host derived molecules released a?ter pathogen and tissue damage,acting as a sentinel for the innate immune system.This article provides an overview of the current concepts regarding the relationship between TLRs signaling and inflammation and calcification remodeling in the pathogenesis of CAVD.The above regulatory mechanisms can provide new targets and strategies for the treatment of CAVD.