Abstract
Autophagy is an important intracellular physiological mechanism that breaks down cytoplasmic organelles and components for energy supply. Autophagy also monitors cells by removing intracellular pathogens, damaged organelles, and abnormally accumulated proteins, which protect cells. Indeed, autophagy preserves and survives the cells by tracking the cytosol. It has been documented that there are relationships between autophagy and autoimmune diseases such as rheumatoid arthritis (RA). Autophagy is involved in various processes such as the development, survival, and proliferation of immune cells, thereby playing an important role in the pathogenesis of RA. In addition, autophagy is implicated in the process of protein citrullination, which is an important process in RA. It has been found that autophagy participates in the presentation of citrullinated peptides through MHC molecules to T lymphocytes, leading to immune response and chronic inflammation in RA. Furthermore, the body of evidence shows that autophagy enhances apoptosis resistance, and increases osteoclastogenesis (destruction of bone tissue), which ultimately leads to severe destruction of bone and cartilage. Due to the important role of autophagy in RA pathogenesis, we investigated the role of autophagy in important mechanisms involved in RA. This review article presents the autophagy involvement in mechanisms such as protein citrullination, osteoclastogenesis, survival of immune cells, apoptosis resistance, lymphocyte homeostasis, and its role in the clinical manifestations of RA.
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Copyright
© 2024, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.