Молекулярные и клеточные механизмы воспаления при подагре: Molecular and cell mechanisms of inflammation in gout

  title={Молекулярные и клеточные механизмы воспаления при подагре: Molecular and cell mechanisms of inflammation in gout},
  author={I. Yu. Malyshev and A. E. Pihlak and O. P. Budanova},
The review analyzes mechanisms of gouty inflammation and resolution of acute inflammation in gout and shows how their understanding contributes to creation of new technologies for the treatment of gout. The first part of the review addresses crystal-induced inflammation in gout, which is associated with activation of the NLRP3 inflammasome in macrophages. The crystal-induced inflammation consists of two stages, 1) synthesis of inflammasome components and 2) inflammasome assembly. The review… 


Gout-associated uric acid crystals activate the NALP3 inflammasome
It is shown that MSU and CPPD engage the caspase-1-activating NALP3 (also called cryopyrin) inflammasome, resulting in the production of active interleukin (IL)-1β and IL-18 in mice deficient in the IL-1β receptor.
Inflammation in gout: mechanisms and therapeutic targets
This Review highlights recent advances in the understanding of both positive and negative regulatory pathways, as well as the genetic and environmental factors that modulate the inflammatory response.
Crystal‐induced neutrophil activation
This review focuses on the current state of knowledge concerning the activation of human neutrophils by MSU crystals specifically in the context of acute gout, as recent data begin to draw a comprehensive picture of the events leading to the often excessive functional responses of neutrophil responses to these particulate agonists.
Epigallocatechin gallate inhibits urate crystals-induced peritoneal inflammation in C57BL/6 mice.
Investigation of the effect of EGCG on MSU-induced inflammation and NLRP3 inflammasome activation indicates that E GCG exerts anti-inflammatory effect against MSU -induced acute gout attack.
Morin, a Bioflavonoid Suppresses Monosodium Urate Crystal-Induced Inflammatory Immune Response in RAW 264.7 Macrophages through the Inhibition of Inflammatory Mediators, Intracellular ROS Levels and NF-κB Activation
The results collectively suggest that morin can be a potential therapeutic agent for inflammatory disorders like acute gouty arthritis.
Annexin A1 promotes timely resolution of inflammation in murine gout
AnxA1 plays a crucial role in the context of acute gouty inflammation by promoting timely resolution of inflammation and increasing neutrophils apoptosis and shortened resolution intervals is studied.
Rebamipide Suppresses Monosodium Urate Crystal-Induced Interleukin-1β Production Through Regulation of Oxidative Stress and Caspase-1 in THP-1 Cells
It is demonstrated that rebamipide inhibits IL-1β activation through suppression of ROS-mediated NF-κB signaling pathways and caspase-1 activation in MSU crystal-induced inflammation.
NLRP3 inflammasome-mediated neutrophil recruitment and hypernociception depend on leukotriene B(4) in a murine model of gout.
The role of the NLRP3 inflammasome is revealed in mediating MSU crystal-induced inflammation and dysfunction of the joints, and the previously unrecognized role of LTB(4) is highlighted in driving NLRP 3 inflammaome activation in response to MSU crystals, both in vitro and in vivo.
NLRP3 activation and mitosis are mutually exclusive events coordinated by NEK7, a new inflammasome component
It is found that activation of the NLRP3 inflammasome was restricted to interphase of the cell cycle by NEK7, a serine-threonine kinase previously linked to mitosis.
Inflammasome-independent regulation of IL-1-family cytokines.
The inflammasome-independent enzymatic processes that are able to activate IL-1 cytokines are reviewed, paying special attention to neutrophil-derived serine proteases, which subsequently induce inflammation and modulate host defense.