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Abstract
Autophagy may have dual roles in gouty arthritis, with preserved autophagic flux potentially aiding inflammatory resolution.
- The effects of autophagy in gouty arthritis are determined by the integrity of autophagic flux rather than just its activation.
- Preserved autophagic flux is associated with reduced inflammation, while impaired autophagic degradation may lead to increased inflammasome activation and joint damage.
- Different cell types, including neutrophils, monocytes/macrophages, chondrocytes, and osteoblasts, exhibit varied autophagy responses based on distinct signaling pathways.
- Challenges exist in interpreting autophagic flux and its implications for inflammation in gout.
- Emerging pharmacological and molecular regulators of autophagy may offer new avenues for targeted therapies in gouty arthritis.
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