1 VCU Pauley Heart Center, Virginia Commonwealth University , Richmond, Virginia.
Antioxid Redox Signal. 2015 May 1;22(13):1146-61. doi: 10.1089/ars.2014.5989. Epub 2014 Dec 11.
An inflammatory response follows an injury of any nature, and while such a response is an attempt to promote healing, it may, itself, result in further injury.
The inflammasome is a macromolecular structure recently recognized as a central mediator in the acute inflammatory response. The inflammasome senses the injury and it amplifies the response by leading to the release of powerful pro-inflammatory cytokines, interleukin-1β (IL-1β) and IL-18.
The activation of the inflammasome in the heart during ischemic and nonischemic injury represents an exaggerated response to sterile injury and promotes adverse cardiac remodeling and failure.
Pilot clinical trials have explored blockade of the inflammasome-derived IL-1β and have shown beneficial effects on cardiac function. Additional clinical studies testing this approach are warranted. Moreover, specific inflammasome inhibitors that are ready for clinical use are currently lacking.
任何性质的损伤都会引发炎症反应，而这种反应虽然是促进愈合的尝试，但它本身可能会导致进一步的损伤。
炎症小体是一种最近被认为是急性炎症反应的中心介质的大分子结构。炎症小体感知损伤，并通过导致强大的促炎细胞因子白细胞介素-1β（IL-1β）和 IL-18 的释放来放大反应。
在缺血性和非缺血性损伤期间，炎症小体在心脏中的激活代表了对无菌损伤的过度反应，并促进了不良的心脏重构和衰竭。
临床试验已经探索了炎症小体衍生的白细胞介素-1β的阻断，并显示对心脏功能有有益的影响。需要进行更多的临床试验来测试这种方法。此外，目前缺乏可用于临床的特定炎症小体抑制剂。
