Inflammation in Fibrodysplasia Ossificans Progressiva and Other Forms of Heterotopic Ossification.

Autor: Matsuo K; Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA.; Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA.; The Program in Craniofacial Biology, University of California, CA, San Francisco, USA., Chavez RD; Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA.; Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA.; The Program in Craniofacial Biology, University of California, CA, San Francisco, USA., Barruet E; Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA.; Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA.; The Program in Craniofacial Biology, University of California, CA, San Francisco, USA., Hsiao EC; Division of Endocrinology and Metabolism, University of California, 513 Parnassus Ave., HSE901, San Francisco, CA, 94143-0794, USA. Edward.hsiao@ucsf.edu.; Department of Medicine, The Institute for Human Genetics, University of California, CA, San Francisco, USA. Edward.hsiao@ucsf.edu.; The Program in Craniofacial Biology, University of California, CA, San Francisco, USA. Edward.hsiao@ucsf.edu.
Jazyk: angličtina
Zdroj: Current osteoporosis reports [Curr Osteoporos Rep] 2019 Dec; Vol. 17 (6), pp. 387-394.
DOI: 10.1007/s11914-019-00541-x
Abstrakt: 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.
Databáze: MEDLINE
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