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REVIEW ARTICLE
Year : 2013  |  Volume : 8  |  Issue : 4  |  Page : 170-178

Pathogenesis of myositis: Lessons learned from animal studies


1 Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington DC; Institute for Biomedical Sciences, The George Washington University, 2300 Eye Street NW, Ross Hall 605, Washington DC, USA
2 Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington DC, USA
3 Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington DC, USA; Department of Integrative Systems Biology; Institute for Biomedical Sciences, The George Washington University, 2300 Eye Street NW, Ross Hall 605, Washington DC, USA

Correspondence Address:
Kanneboyina Nagaraju
Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington DC, USA; Department of Integrative Systems Biology; Institute for Biomedical Sciences, The George Washington University, 2300 Eye Street NW, Ross Hall 605, Washington DC, USA

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Source of Support: None, Conflict of Interest: None


DOI: 10.1016/j.injr.2013.09.006

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Recent studies have continued to clarify the pathogenic mechanisms responsible for muscle damage and weakness in inflammatory myopathies. Traditionally, adaptive im- mune mechanisms such as cell mediated (cytotoxic) and humoral (autoantibodies and complement) components have been implicated in the pathogenesis of polymyositis/in- clusion body myositis and dermatomyositis, respectively. However, recent studies have shown a significant overlap of immune components in these disorders. Likewise, studies have provided evidence not only for adaptive immune pathogenic mechanisms but also for innate immune, such as the TLR-NF-kB signaling, and non-immune mechanisms, such as endoplasmic reticulum stress response, autophagy, metabolic deficits in ATP generating pathways and hypoxia. These recent studies indicate that the muscle fiber damage and weakness in myositis may not be solely mediated by an adaptive immune attack (e.g., autoreactive CTLs or autoantibodies) but also mediated through innate immune and metabolic mechanisms. In this review, we have briefly outlined the current developments in immune (adaptive, innate) and non-immune components of disease pathogenesis in inflammatory myopathies.


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