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July 4, 2024Annals of the Rheumatic Diseases68 citationsOpen Access

Acod1-mediated inhibition of aerobic glycolysis suppresses osteoclast differentiation and attenuates bone erosion in arthritis

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KKKaterina KachlerDADarja AndreevSTShreeya Thapa

Key Points

  • Aconitate decarboxylase 1 mediates metabolic suppression of aerobic glycolysis to inhibit osteoclast differentiation and reduce arthritic bone erosion.
  • The metabolic regulator itaconate and its producing enzyme link monocyte lineage cell state directly to the restriction of inflammatory bone destruction.
  • Investigation of monocyte-derived cells highlights Acod1 pathways as potential metabolic targets for treating bone loss in rheumatoid arthritis models.

Abstract

Metabolic changes are crucially involved in osteoclast development and may contribute to bone degradation in rheumatoid arthritis (RA). The enzyme aconitate decarboxylase 1 (Acod1) is known to link the cellular function of monocyte-derived macrophages to their metabolic status. As osteoclasts derive from the monocyte lineage, we hypothesised a role for Acod1 and its metabolite itaconate in osteoclast differentiation and arthritis-associated bone loss.

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Cite This Study

Kachler et al. (2024) studied this question.

synapsesocial.com/papers/68e615d4b6db6435875a8147https://doi.org/10.1136/ard-2023-224774
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