Dysregulation of Different Modes of Programmed Cell Death in Rheumatoid Arthritis Fibroblast-Like Synoviocyte

Area of Science:

• Immunology
• Pathology
• Rheumatology

Background:

• Rheumatoid arthritis (RA) is a chronic inflammatory joint disease with complex pathogenesis.
• Despite available treatments like NSAIDs, DMARDs, and bDMARDs, suboptimal outcomes persist for some RA patients.
• Programmed cell death (PCD) is increasingly recognized as a critical factor in RA pathophysiology.

Purpose of the Study:

• To systematically review the roles of diverse cell death modalities in rheumatoid arthritis.
• To explore how dysregulated PCD contributes to RA progression and joint damage.
• To identify potential new therapeutic targets and inform drug development for RA.

Main Methods:

• Literature review of programmed cell death (PCD) in rheumatoid arthritis (RA).
• Analysis of various cell death pathways: apoptosis, necroptosis, ferroptosis, pyroptosis, and autophagy.
• Synthesis of current understanding of PCD's impact on RA pathogenesis.

Main Results:

• Dysregulation of multiple PCD pathways, including apoptosis, necroptosis, ferroptosis, pyroptosis, and autophagy, is implicated in RA.
• These cell death modalities significantly influence the chronic synovitis and joint deformities characteristic of RA.
• Understanding these mechanisms provides insights into RA's complex pathophysiology.

Conclusions:

• Targeting specific programmed cell death (PCD) pathways presents a promising strategy for novel RA therapies.
• Further research into the interplay of different cell death modalities in RA is warranted.
• This review provides a foundation for developing more effective treatments for rheumatoid arthritis.