Both immune and non-immune mechanisms are involved in muscle damage and dysfunction occurring in idiopathic inflammatory myopathies (IIMs). Crosstalk among inflammatory cells, muscle and endothelial cells is essential in the pathogenesis of IIMs. Resistin, originally described as an adipokine linking obesity and insulin resistance in rodents, has been shown a pro-inflammatory molecule in humans. Besides its direct effect on production of several inflammatory mediators, resistin influences chemotaxis, migration, proliferation, cell survival, endothelial dysfunction and metabolism--all aspects implicated in the pathogenesis of IIMs. Up-regulation of resistin in muscle tissue and elevated serum resistin levels have been recently demonstrated in patients with IIMs. In addition, serum levels of resistin reflected global disease activity, including extramuscular organ involvement, in patients with this disease. However, there are currently not sufficient data to distinguish the features of resistin that cause injury of muscle tissue from those that promote muscle regeneration and repair. The aim of this review is therefore to summarize current knowledge about potential implication of resistin in idiopathic inflammatory myopathies.

• MeSH
• biologické markery metabolismus   MeSH
• cévní endotel metabolismus   patologie   MeSH
• chemotaxe fyziologie   MeSH
• cytokiny metabolismus   MeSH
• endoteliální buňky metabolismus   patologie   MeSH
• lidé MeSH
• myozitida krev   etiologie   patologie   MeSH
• pohyb buněk fyziologie   MeSH
• proliferace buněk MeSH
• resistin fyziologie   MeSH
• upregulace MeSH
• viabilita buněk fyziologie   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• biologické markery MeSH
• cytokiny MeSH
• resistin MeSH
• RETN protein, human MeSH Prohlížeč