ArticleCellular and molecular life sciences : CMLS2024
Disturbed glycolipid metabolism activates CXCL13-CXCR5 axis in senescent TSCs to promote heterotopic ossification.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- The CXCL13 hub in obesity-related metabolic inflammation: regulation of spatiotemporal heterogeneity and targeted strategies.The Journal of endocrinology · 2026Review
- ROS-responsive Ganoderma lucidum polysaccharide nanocomposite targeting prosenescent oxidative stress niche for structural and functional diabetic tendon regeneration.Journal of nanobiotechnology · 2026Article
- Inflammaging and Senescence-Associated Secretory Phenotype (SASP) in Psoriasis - A Narrative Review of Potential Mechanisms and Anti-Inflammaging Strategies.Psoriasis (Auckland, N.Z.) · 2026Review
- From fat to fate: how aging adipose tissue drives systemic metabolic aging.Biogerontology · 2025Review
- Molecular basis of individual locomotor function: Integrated understanding of gene expression regulation in the development and homeostasis of the musculoskeletal system.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Review
- The impact of diabetes mellitus on tendon pathology: a review.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Heterotopic ossification (HO) occurs as a common complication after injury, while its risk factor and mechanism remain unclear, which restricts the development of pharmacological treatment. Clinical research suggests that diabetes mellitus (DM) patients are prone to developing HO in the tendon, but solid evidence and mechanical research are still needed. Here, we combined the clinical samples and the DM mice model to identify that disordered glycolipid metabolism aggravates the senescence of tendon-derived stem cells (TSCs) and promotes osteogenic differentiation. Then, combining the RNA-seq results of the aging tendon, we detected the abnormally activated autocrine CXCL13-CXCR5 axis in TSCs cultured in a high fat, high glucose (HFHG) environment and also in the aged tendon. Genetic inhibition of CXCL13 successfully alleviated HO formation in DM mice, providing a potential therapeutic target for suppressing HO formation in DM patients after trauma or surgery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.