炎性骨溶解：一场针对骨骼的“阴谋”。
Inflammatory osteolysis: a conspiracy against bone.
作者信息
Mbalaviele Gabriel, Novack Deborah V, Schett Georg, Teitelbaum Steven L
机构信息
Department of Medicine, Division of Bone and Mineral Diseases, and.
Department of Pathology and Immunology, Division of Anatomic and Molecular Pathology, Washington University School of Medicine, St. Louis, Missouri, USA.
出版信息
J Clin Invest. 2017 Jun 1;127(6):2030-2039. doi: 10.1172/JCI93356.
Abstract
There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorptive cell or do so indirectly via cytokine arrest. Despite these advances, a substantial number of patients with inflammatory arthritis remain resistant to current therapies, and even effective anti-inflammatory drugs frequently do not repair damaged bone. Thus, insights into events such as those impacted by inflammasomes, which signal through cytokine-dependent and -independent mechanisms, are needed to optimize treatment of inflammatory osteolysis.
摘要
炎症性骨溶解有多种病因，但无论病因和细胞环境如何，破骨细胞都是降解骨组织的细胞。因此，炎性细胞因子对破骨细胞形成和功能的影响是推进局灶性骨溶解治疗的最重要发现之一，促使了直接阻断骨吸收细胞或通过细胞因子阻滞间接阻断骨吸收细胞的治疗药物的研发。尽管有这些进展，但仍有相当数量的炎性关节炎患者对当前治疗有抗性，甚至有效的抗炎药物也常常无法修复受损骨骼。因此，需要深入了解诸如受炎性小体影响的事件，这些事件通过细胞因子依赖性和非依赖性机制发出信号，以优化炎症性骨溶解的治疗。
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2
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3
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