The NLRP3 inflammasome - interleukin 1 pathway as a therapeutic target in gout

被引：70

作者：

Szekanecz, Zoltan ^{[1
]}

Szamosi, Szilvia ^{[1
]}

Kovacs, Gergo E. ^{[2
]}

Kocsis, Elek ^{[2
]}

Benko, Szilvia ^{[2
]}

机构：

[1] Univ Debrecen, Fac Med, Dept Med, Div Rheumatol, Debrecen, Hungary

[2] Univ Debrecen, Fac Med, Dept Physiol, Debrecen, Hungary

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2019年 / 670卷

关键词：

Inflammasome; NLRP3; Interleukin; 1; Gout; Autoinflammatory disease; EVIDENCE-BASED RECOMMENDATIONS; CRYSTAL-INDUCED INFLAMMATION; URIC-ACID; DOUBLE-BLIND; METABOLIC-DISORDER; NALP3; INFLAMMASOME; XANTHINE-OXIDASE; MURINE MODEL; LIFE-STYLE; K+ EFFLUX;

D O I：

10.1016/j.abb.2019.01.031

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The NLRP3 inflammasome is implicated in the processing of the pro-inflammatory cytokine interleukin 1 beta. Inflammatory disorders associated with the activation of the NLRP3 inflammasome - IL-1 axis are termed autoinflammatory diseases. Gout is an autoinflammatory disease, which is triggered by the deposition of monosodium urate crystals of precipitated uric acid. It is characterized by recurrent attacks of inflammation due to the activation of phagocytic cells that try to clear the crystals. NLRP3 inflammasome-mediated IL-1 beta production plays a key role in the manifestation of the disease. Currently, the best approach to treat gout is to reduce uric acid concentration by targeting xanthine oxidase or uric acid transporters, or to use non-steroidal anti-inflammatory drugs. Nevertheless, most of these treatments are not effective enough and may results in side effects. During the past decades, our knowledge has greatly improved about the molecular mechanisms of NLRP3 activation. This knowledge enables and urges scientists to discover or design drugs that target pathways of NLRP3 inflammasome activation, or more preferentially, NLRP3 inflammasome itself. In this review, we discuss the already available drugs and products, that target the diverse pathways of the NLRP3 - IL-1 beta axis, and the future therapeutic perspectives.

引用

页码：82 / 93

页数：12

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