期刊
SKELETAL MUSCLE
卷 3, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/2044-5040-3-13
关键词
Adaptive immune; Autophagy; Cytokines; Endoplasmic reticulum stress; Innate immune; Myositis; Skeletal muscle; TLRs
类别
资金
- NIH [RO1-AR050478, 5U54HD053177, K26OD011171]
- Muscular Dystrophy Association
- US Department of Defense [W81XWH-05-1-0616]
- Association Francaise Contreles Myopathies
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [K26OD011171] Funding Source: NIH RePORTER
Idiopathic inflammatory myopathies (IIMs) are a heterogenous group of complex muscle diseases of unknown etiology. These diseases are characterized by progressive muscle weakness and damage, together with involvement of other organ systems. It is generally believed that the autoimmune response (autoreactive lymphocytes and autoantibodies) to skeletal muscle-derived antigens is responsible for the muscle fiber damage and muscle weakness in this group of disorders. Therefore, most of the current therapeutic strategies are directed at either suppressing or modifying immune cell activity. Recent studies have indicated that the underlying mechanisms that mediate muscle damage and dysfunction are multiple and complex. Emerging evidence indicates that not only autoimmune responses but also innate immune and non-immune metabolic pathways contribute to disease pathogenesis. However, the relative contributions of each of these mechanisms to disease pathogenesis are currently unknown. Here we discuss some of these complex pathways, their inter-relationships and their relation to muscle damage in myositis. Understanding the relative contributions of each of these pathways to disease pathogenesis would help us to identify suitable drug targets to alleviate muscle damage and also improve muscle weakness and quality of life for patients suffering from these debilitating muscle diseases.
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