Inflammation in Fibrodysplasia Ossificans Progressiva and Other Forms of Heterotopic Ossification

被引:46
|
作者
Matsuo, Koji [1 ,2 ,3 ]
Chavez, Robert Dalton [1 ,2 ,3 ]
Barruet, Emilie [1 ,2 ,3 ]
Hsiao, Edward C. [1 ,2 ,3 ]
机构
[1] Univ Calif San Francisco, Div Endocrinol & Metab, 513 Parnassus Ave,HSE901, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Med, Inst Human Genet, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Program Craniofacial Biol, San Francisco, CA 94143 USA
关键词
Heterotopic ossification; Inflammation; Immune activation; Macrophages; Cytokines; OSTEOCLAST DIFFERENTIATION FACTOR; VASCULAR SMOOTH-MUSCLE; BONE-FORMATION; RISK-FACTORS; CELLS; MACROPHAGES; BMP; RECEPTOR; TRAUMA; GROWTH;
D O I
10.1007/s11914-019-00541-x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review Heterotopic ossification (HO) is associated with inflammation. The goal of this review is to examine recent findings on the roles of inflammation and the immune system in HO. We examine how inflammation changes in fibrodysplasia ossificans progressiva, in traumatic HO, and in other clinical conditions of HO. We also discuss how inflammation may be a target for treating HO. Recent findings Both genetic and acquired forms of HO show similarities in their inflammatory cell types and signaling pathways. These include macrophages, mast cells, and adaptive immune cells, along with hypoxia signaling pathways, mesenchymal stem cell differentiation signaling pathways, vascular signaling pathways, and inflammatory cytokines. Because there are common inflammatory mediators across various types of HO, these mediators may serve as common targets for blocking HO. Future research may focus on identifying new inflammatory targets and testing combinatorial therapies based on these results.
引用
收藏
页码:387 / 394
页数:8
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