title: The Role of Autophagy in Rheumatic Disease.
abstract: Autophagy is an evolutionarily conserved degradation process in triggered by metabolic stress or environmental changes. Autophagy involves formation of autophagosomes, which fuse with lysosomes and degrade encapsulated intracellular components, such as long-lived and misfolded proteins, as well as intracellular organelles. Autophagy has been implicated in a wide variety of physiological and pathological conditions, and was recently implicated in the regulation of immunity and inflammation. Rheumatic diseases are a group of disorders characterized by immune system malfunctions in which the body attacks its own tissues. These diseases can seriously threaten human health if untreated. Although the underlying pathophysiology of autoimmune diseases has not yet been fully elucidated, autophagy has been implicated in their progression. In this article, we review the basics of autophagy, and the functional role of autophagy in the pathogenesis of rheumatic diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Crohn's disease and ankylosing spondylitis (AS). Moreover, we reviewed the role of autophagy and autophagy-related genes (Atgs) in innate and adaptive immunity, as well as the pathogenic crosstalk between autophagy and apoptosis. Our findings should provide valuable insights into the role of autophagy in the pathogenesis of rheumatic diseases. In addition, identification of novel autophagy-associated target proteins may offer a promising target for drugs treating human rheumatic disorders.
authors.affiliation: Department of Clinical Immunology, State Key Discipline of Cell Biology, Xijing Hospital, Fourth Military Medical University, Xi`an, Shaanxi Province, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Feng
authors.affiliation: Department of Orthopedics, Forty-second Hospital of Chinese People`s Liberation Army, Leshan, Sichuan Province, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Li
authors.affiliation: Department of Clinical Immunology, State Key Discipline of Cell Biology, Xijing Hospital, Fourth Military Medical University, Xi`an, Shaanxi Province, China.
authors.forename: Xue Yi
authors.initials: XY
authors.lastname: Li
authors.affiliation: Department of Clinical Immunology, State Key Discipline of Cell Biology, Xijing Hospital, Fourth Military Medical University, Xi`an, Shaanxi Province, China.
authors.forename: Zhen Biao
authors.initials: ZB
authors.lastname: Wu
mesh_terms: D056704:Adaptive Immunity / Q000276:immunology; D000818:Animals; D018501:Antirheumatic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000276:immunology; D001343:Autophagy / Q000276:immunology*; D015195:Drug Design; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D058990:Molecular Targeted Therapy; D012216:Rheumatic Diseases / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*
chemical_list: D018501:Antirheumatic Agents
keywords: Autophagy; Crohn's disease; ankylosing spondylitis; pathogenesis; rheumatic disease; rheumatoid arthritis; systemic lupus erythematosus.