ArticleFrontiers in medicine2026
ACADL and ADH1B signify ketone body metabolic reprogramming in osteoarthritic synovium: insights from bioinformatics and animal model studies.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Osteoarthritis (OA) is characterized by articular degeneration and chronic joint pain, partly resulting from synovial inflammation. Accumulating evidence suggests that alterations in the synovial ketone body metabolism (KBM) are closely associated with OA pathogenesis. This study aimed to investigate the metabolic changes in synovial tissues to optimize the treatment of clinical OA. Methods: Analysis of OA and normal control synovial transcriptomic datasets extracted from the Gene Expression Omnibus (GEO) identified 808 differentially expressed genes (DEGs). These DEGs were integrated with KBM-related genes from the metabolic databases, yielding 50 candidates related to OA progression. Following enrichment analysis, protein-protein interaction network construction via STRING, and machine learning with expression analysis, two genes were identified as OA biomarkers: ACADL, encoding long-chain acyl-CoA dehydrogenase and Results: The nomogram based on these data revealed high accuracy in the training and validation sets. Functional analysis revealed that these genes function in lipid oxidation, a process critical for synovial cell energy metabolism, as well as in the redox balance that prevents oxidative stress from worsening OA inflammation. Immune infiltration analysis revealed that their expression significantly correlated with 21 immune subtypes, including pro-inflammatory M1 macrophages and Th17 cells, which drive synovial inflammation. Molecular docking analysis identified progesterone and fomepizole as potential agents with satisfactory affinities for Discussion:
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