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October 11, 2025Molecular MedicineOpen Access

Dysfunctional glycolysis-UCP2-fatty acid oxidation promotes CTLA4intFOXP3int regulatory T-cell production in rheumatoid arthritis

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Authors

JHJiawen HanZZZhongyang ZhouHWHongxia Wang

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Overview

Analysis reveals metabolic dysfunction in Tregs influences CTLA4 dynamics, suggesting UCP2 as a target.

Key Points

  • Dysfunctional glycolysis and UCP2 elevation in Tregs contribute to impaired CTLA4 levels, impacting immune function.
  • UCP2 suppression improved Treg function in RA, as shown by restored CTLA4 presence and reduced inflammation.
  • This study utilized a chimeric mouse model to investigate the roles of UCP2 and FAO in Treg metabolism.
  • Understanding these pathways supports potential UCP2-targeted therapies to treat rheumatoid arthritis.

Cite This Study

Han et al. (2025) studied this question.

synapsesocial.com/papers/68ea72339f1bd4df558cec35https://doi.org/10.1186/s10020-025-01372-6
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