期刊
CURRENT OPINION IN RHEUMATOLOGY
卷 21, 期 6, 页码 581-587出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0b013e3283319265
关键词
autophagy; cell death; endoplasmic reticulum; idiopathic myopathy; myositis; nuclear factor-kappa B activation; skeletal muscle
类别
资金
- National Institutes of Health [R01-AR050478, 5t754HD053177]
- Foundation to Eradicate Dystrophy
- United States Department of Defense [W81Xt'ffl-05-1-0616]
- Myositis Association
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brazil
Purpose of review Recent literature in inflammatory myopathies suggests that both immune (cell-mediated and humoral) and nonimmune [endoplasmic reticulum (ER) stress and autophagy] mechanisms play a role in muscle fiber damage and dysfunction. This review describes these findings and discusses their relevance to disease pathogenesis and therapy. Recent findings Recent studies highlight the role of ER stress response, especially the roles of hexose-6-phosphate dehydrogenase and ER-anchored RING finger E3 ligase in the activation of unfolded protein response and the formation of vacuoles and inclusions in myopathies. Several studies investigated the link between inflammation and the beta-amyloid-associated muscle fiber degeneration and loss of muscle function. Likewise, the roles of ER stress and autophagy in skeletal muscle damage have been explored in multiple muscle diseases. Summary Current data indicate that the ER stress, nuclear factor-kappa B pathway and autophagy are active in the skeletal muscle of myositis patients, and the proinflammatory nuclear factor-kappa B pathway connects the immune and nonimmune pathways of muscle damage. The relative contributions of each of these pathways to muscle fiber damage are currently unclear. Therefore, further defining the role of these pathways in disease pathogenesis should help to design effective therapeutic agents for these diseases.
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