Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases

Area of Science:

• Cell Biology
• Immunology
• Biochemistry

Background:

• The endoplasmic reticulum (ER) maintains cellular homeostasis, protein synthesis, folding, and secretion.
• Loss of ER homeostasis is increasingly linked to autoimmune inflammatory disorders, particularly rheumatic diseases.
• ER stress is a key factor in the pathogenesis of rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE).

Purpose of the Study:

• To review the role of ER stress in the pathogenesis of rheumatic diseases, focusing on RA and SLE.
• To explore the interplay between protein folding, reactive oxygen species (ROS), and oxidative stress (OS) in ER stress.
• To examine intervention studies targeting ER stress and OS in rheumatic diseases.

Main Methods:

• Literature review of current knowledge on ER stress in rheumatic diseases.
• Analysis of the relationship between ER stress, protein misfolding, and oxidative stress.
• Evaluation of therapeutic strategies targeting ER stress and OS.

Main Results:

• ER stress significantly contributes to the pathogenesis of RA and SLE.
• A vicious cycle exists where ER stress induces OS, which exacerbates protein misfolding and oxidation.
• Intervention studies targeting ER stress and OS pathways show promising results in preclinical models.

Conclusions:

• Loss of ER homeostasis is a critical factor in RA and SLE pathogenesis.
• Targeting ER stress, unfolded protein response (UPR) pathways, and OS demonstrates therapeutic potential.
• Further investigation of these targets in vitro and in animal models is warranted.