首页> 美国卫生研究院文献>other >Regulatory Mechanisms of the NLRP3 Inflammasome a Novel Immune-Inflammatory Marker in Cardiovascular Diseases
【2h】

Regulatory Mechanisms of the NLRP3 Inflammasome a Novel Immune-Inflammatory Marker in Cardiovascular Diseases

机译:NLRP3炎性小体心血管疾病中的新型免疫炎症标记物的调节机制。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

The nod-like receptor family pyrin domain containing 3 (NLRP3) is currently the most widely studied inflammasome and has become a hot topic of recent research. As a macromolecular complex, the NLRP3 inflammasome is activated to produce downstream factors, including caspase-1, IL-1β, and IL-18, which then promote local inflammatory responses and induce pyroptosis, leading to unfavorable effects. A growing number of studies have examined the relationship between the NLRP3 inflammasome and cardiovascular diseases (CVDs). However, some studies have shown that the NLRP3 inflammasome is not involved in the occurrence of certain diseases. Therefore, identifying the mechanism of action of the NLRP3 inflammasome and its potential involvement in the pathological process of disease progression is of utmost importance. This review discusses the mechanisms of NLRP3 inflammasome activation and the relationship between the inflammasome and CVDs, including coronary atherosclerosis, myocardial ischemia/reperfusion, cardiomyopathies, and arrhythmia, as well as CVD-related treatments.
机译:包含3的nod样受体家族吡啶结构域(NLRP3)是目前研究最广泛的炎症小体,已成为近期研究的热点。作为大分子复合物,NLRP3炎性小体被激活以产生下游因子,包括caspase-1,IL-1β和IL-18,这些因子随后会促进局部炎症反应并诱发细胞凋亡,从而导致不良影响。越来越多的研究检查了NLRP3炎性体与心血管疾病(CVD)之间的关系。但是,一些研究表明,NLRP3炎性体不参与某些疾病的发生。因此,最重要的是确定NLRP3炎性小体的作用机理及其潜在参与疾病进展的病理过程。这篇综述讨论了NLRP3炎性体激活的机制以及炎性体与CVD之间的关系,包括冠状动脉粥样硬化,心肌缺血/再灌注,心肌病和心律不齐,以及与CVD相关的治疗。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号