Nonimmune mechanisms in idiopathic inflammatory myopathies
| Autor: | Marta Loredo Martinez, Anna Ghirardello, Sandra Zampieri, Chiara Franco, Andrea Doria, Mariele Gatto |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Muscle Fibers Skeletal Inflammation Neuromuscular junction Pathogenesis 03 medical and health sciences 0302 clinical medicine Rheumatology Autophagy medicine Humans 030203 arthritis & rheumatology Denervation Myositis business.industry Toll-Like Receptors Endoplasmic Reticulum Stress 030104 developmental biology medicine.anatomical_structure TLR3 Immunology Unfolded protein response medicine.symptom Reactive Oxygen Species business Interferon type I medicine.drug |
| Zdroj: | Current Opinion in Rheumatology. 32:515-522 |
| ISSN: | 1531-6963 1040-8711 |
| DOI: | 10.1097/bor.0000000000000748 |
| Popis: | Purpose of review This review encompasses the main novelties regarding nonimmune mechanisms implicated in the pathogenesis of idiopathic inflammatory myopathies (IIM). Recent findings In recent years, growing data support a role for endoplasmic-reticulum (ER) stress as a propagator of muscular damage, together with the release of interferon type I and reactive oxygen species in hypoxemic muscle fibers. Other studies evaluating the relationship between autophagy and Toll-like receptors (TLRs) in IIM subtypes have shown increased TLR3 and TLR4 expression in fibers of IIM patients and colocalization with LC3, an autophagy marker, submitting autophagy as a likely player in IIM pathogenesis. Most novel evidences concern the potential role of denervation of the neuromuscular junction in IIM, possibly connected to hyperexpression of MHC-I, and trafficking of extracellular vesicles, which may represent a connection between nonimmune and immune-mediated mechanisms of muscle inflammation and damage. Summary Nonimmune mechanisms contribute to the pathogenesis of IIM, likely cooperating with immune-mediated inflammation. Consistent data were released for ER stress, autophagy, mitochondrial dysfunction and hypoxia; in addition to, neuromuscular denervation and extracellular vesicles have been proposed as thoughtful links between muscle inflammation, damage and atrophy. Further understanding of nonimmune abnormalities and potential reversible pathways is needed to improve the management of IIM. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|