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.
Keywords: Autophagy, rheumatic disease, pathogenesis, systemic lupus erythematosus, rheumatoid arthritis, Crohn's disease,
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