Omnipresence of inflammasome activities in inflammatory bone diseases

被引:43
作者
Alippe, Yael [1 ]
Mbalaviele, Gabriel [1 ]
机构
[1] Washington Univ, Div Bone & Mineral Dis, Sch Med, 660 South Euclid Ave,Campus Box 8301, St Louis, MO 63110 USA
关键词
Inflammation; Inflammasomes; Osteoclasts; Bone resorption; NLRP3; Cytokines; KAPPA-B LIGAND; NECROSIS-FACTOR-ALPHA; JUVENILE IDIOPATHIC ARTHRITIS; RECEPTOR ANTAGONIST ANAKINRA; NLRP3; INFLAMMASOME; GASDERMIN D; RHEUMATOID-ARTHRITIS; NALP3; OSTEOCLAST DIFFERENTIATION; CAUSES AUTOINFLAMMATION;
D O I
10.1007/s00281-019-00753-4
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The inflammasomes are intracellular protein complexes that are assembled in response to a variety of perturbations including infections and injuries. Failure of the inflammasomes to rapidly clear the insults or restore tissue homeostasis can result in chronic inflammation. Recurring inflammation is also provoked by mutations that cause the constitutive assembly of the components of these protein platforms. Evidence suggests that chronic inflammation is a shared mechanism in bone loss associated with aging, dysregulated metabolism, autoinflammatory, and autoimmune diseases. Mechanistically, inflammatory mediators promote bone resorption while suppressing bone formation, an imbalance which over time leads to bone loss and increased fracture risk. Thus, while acute inflammation is important for the maintenance of bone integrity, its chronic state damages this tissue. In this review, we discuss the role of the inflammasomes in inflammation-induced osteolysis.
引用
收藏
页码:607 / 618
页数:12
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