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Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification formation

GSE234916 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2024/08/28 Platform GPL24247
Summary
Heterotopic ossification (HO) occurs as a common complication after injury, while its risk factor and mechanism remain unclear yet, which restricts the development of pharmacological treatment. Clinical research suggested that diabetes mellitus (DM) patients were prone to develop HO in tendon, but the solid evidence and mechanical research are still needed. Here, we combined the clinical samples and DM mice model to identify that disordered glycolipid metabolism aggravates the senescence of tendon derived stem cells (TSCs) and promotes their osteogenic differentiation. Then, combining the RNA-seq results of aging tendon, we detected the abnormally activated autocrine CXCL13-CXCR5 axis in TSCs cultured in high fat high glucose (HFHG) environment and also in aged tendon. Genetic inhibition of CXCL13 successfully alleviates the HO formation in DM mice, providing a potential therapeutical target for suppressing HO formation in DM patients after trauma or surgery.
Published in
Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification
Chen Y, Wu J, Wong C et al. · Cellular and molecular life sciences : CMLS 2024 · PMID 38880863 · doi:10.1007/s00018-024-05302-3
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Also filed as BioProject PRJNA983738 and SRA study SRP443351. Searching any of these in the dataset finder brings you back here.

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