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Acod1-mediated effect on osteoclast differentiation

GSE237504 Mus musculus Expression profiling by high throughput sequencing 9 samples Submitted 2024/07/15 Platform GPL24247
Summary
Enhanced osteoclast-mediated bone erosion is a prominent hallmark of rheumatoid arthritis. Emerging evidence suggests that this process is facilitated by metabolic dysregulation of osteoclasts. The mitochondrial enzyme aconitate decarboxylase 1 (Acod1, also known as immune responsive gene 1 [Irg1]) serves as a mediator between the metabolic condition and the functional state of different types of cells. Acod1-deficient mice are characterized by enhanced osteoclast differentiation and bone erosion in an inflammatory arthritis model, while therapeutic treatment with the itaconate-derivative 4-octyl-itaconate (4-OI) alleviates the disease phenotype in experimental arthritis. To ascertain the influence of the Acod1-itaconate axis on the genomic transcriptional network of osteoclasts, we performed a whole transcriptome RNA sequencing analysis with fully differentiated osteoclasts from WT and Acod1-deficient mice that were cultured in the presence or absence of 4-OI.
Published in
Acod1-mediated inhibition of aerobic glycolysis suppresses osteoclast differentiation and attenuates bone erosion in arthritis
Kachler K, Andreev D, Thapa S et al. · Annals of the rheumatic diseases 2024 · PMID 38964754 · doi:10.1136/ard-2023-224774
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Also filed as BioProject PRJNA995539 and SRA study SRP450002. Searching any of these in the dataset finder brings you back here.

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