کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2958976 | 1178305 | 2015 | 8 صفحه PDF | دانلود رایگان |

• The inflammasome is a complex of intracellular interaction proteins that trigger maturation of proinflammatory cytokines IL-1β and IL-18 to initiate the inflammatory response.
• The inflammasome may play a central role in modulating chronic inflammation and in turn affecting heart failure progression.
• Antiinflammatory drug therapy can lead to compromised host defense or further amplification of inflammatory processes owing to the many redundancies and compensatory responses built into this complicated defense system.
• Targeting specific inflammatory pathways, such as NLRP3 activation, may provide a more precise approach to reducing deleterious inflammation in heart failure while leaving some innate host defense intact.
• Further research on targeting the NLRP3 inflammasome in HF patients is warranted.
Patients with heart failure continue to suffer adverse health consequences despite advances in therapies over the past 2 decades. Identification of novel therapeutic targets that may attenuate disease progression is therefore needed. The inflammasome may play a central role in modulating chronic inflammation and in turn affecting heart failure progression. The inflammasome is a complex of intracellular interaction proteins that trigger maturation of proinflammatory cytokines interleukin-1β and interleukin-18 to initiate the inflammatory response. This response is amplified through production of tumor necrosis factor α and activation of inducible nitric oxide synthase. The purpose of this review is to discuss recent evidence implicating this inflammatory pathway in the pathophysiology of heart failure.
Journal: Journal of Cardiac Failure - Volume 21, Issue 7, July 2015, Pages 586–593