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Nat Rev Rheumatol. 2016 Sep;12(9):517-31. doi: 10.1038/nrrheum.2016.92. Epub 2016 Jun 23.

Autophagy: controlling cell fate in rheumatic diseases.

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Arthritis Program, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, Ontario, M5T 2S8, Canada.
Division of Genetics and Development, Krembil Research Institute, University Health Network, 60 Leonard Avenue, Toronto, Ontario, M5T 2R1, Canada.
Department of Surgery, Department of Laboratory Medicine and Pathobiology, University of Toronto, 686 Bay Street, Toronto, Ontario, M5G 0A4, Canada.


Autophagy, an endogenous process necessary for the turnover of organelles, maintains cellular homeostasis and directs cell fate. Alterations to the regulation of autophagy contribute to the progression of various rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), osteoarthritis (OA) and systemic sclerosis (SSc). Implicit in the progression of these diseases are cell-type-specific responses to surrounding factors that alter autophagy: chondrocytes within articular cartilage show decreased autophagy in OA, leading to rapid cell death and cartilage degeneration; fibroblasts from patients with SSc have restricted autophagy, similar to that seen in aged dermal fibroblasts; fibroblast-like synoviocytes from RA joints show altered autophagy, which contributes to synovial hyperplasia; and dysregulation of autophagy in haematopoietic lineage cells alters their function and maturation in SLE. Various upstream mechanisms also contribute to these diseases by regulating autophagy as part of their signalling cascades. In this Review, we discuss the links between autophagy, immune responses, fibrosis and cellular fates as they relate to pathologies associated with rheumatic diseases. Therapies in clinical use, and in preclinical or clinical development, are also discussed in relation to their effects on autophagy in rheumatic diseases.

[Indexed for MEDLINE]

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