Butts Brittany, Gary Rebecca A, Dunbar Sandra B, Butler Javed
Nell Hodgson Woodruff School of Nursing, Emory University, Atlanta, GA.
Cardiology Division, Stony Brook University, Stony Brook, NY.
J Card Fail. 2015 Jul;21(7):586-93. doi: 10.1016/j.cardfail.2015.04.014. Epub 2015 May 14.
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.
尽管在过去20年里治疗方法有所进步,但心力衰竭患者仍继续遭受不良健康后果。因此,需要确定可能减缓疾病进展的新治疗靶点。炎性小体可能在调节慢性炎症进而影响心力衰竭进展中起核心作用。炎性小体是一种细胞内相互作用蛋白复合物,可触发促炎细胞因子白细胞介素-1β和白细胞介素-18的成熟,从而启动炎症反应。这种反应通过肿瘤坏死因子α的产生和诱导型一氧化氮合酶的激活而放大。本综述的目的是讨论最近将这一炎症途径与心力衰竭病理生理学联系起来的证据。