ReviewMolecular biology reports2025
Understanding the role of 14-3-3Ƞ protein in rheumatoid arthritis: from molecular dysregulation to therapeutic Redirection.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic inflammation in the synovial joints, resulting in joint damage and systemic complications. The 14-3-3η protein, a member of the 14-3-3 family of regulatory proteins, has shown promise as a biomarker and a potential therapeutic target for treating RA. High levels of 14-3-3η protein have been consistently detected in the synovial fluid and blood serum of RA patients, showing a relationship with disease severity and joint deterioration. Functionally, 14-3-3η protein interacts with various intracellular signaling pathways that control immune responses, apoptosis, and cell survival. It enhances the production of pro-inflammatory cytokines, which contribute to joint swelling and bone loss in RA. The clinical implications of 14-3-3η protein are substantial. Furthermore, targeting the 14-3-3η protein and its associated pathways, such as MAPK/ERK, SAPK/JNK, and JAK-STAT, offers a new therapeutic strategy for reducing inflammation and preventing joint damage. Recent preclinical research has shown that drugs that inhibit 14-3-3η protein expression levels reduce synovial inflammation and bone loss, highlighting its potential as a disease-modifying intervention in RA.
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