ArticleBulletin of experimental biology and medicine2026
Analysis of SUCNR1 in Cartilage Tissue and Its Association with Succinate Metabolism in the Metabolic Phenotype of Osteoarthritis.
Article in Bulletin of experimental biology and 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
Inflammation disrupts the normal metabolism of chondrocytes, shifting it toward catabolism and thereby accelerating cartilage extracellular matrix degradation. Recent data suggest a possible contribution of succinate-dependent signaling, mediated by the succinate receptor 1 (SUCNR1/GPR91), to these processes. While the involvement of the succinate receptor SUCNR1 in cartilage degeneration is documented, its role in the metabolic phenotype of osteoarthritis remains poorly understood. We conducted a comprehensive assessment of the succinate signaling system in the metabolic phenotype of osteoarthritis by analyzing SUCNR1 expression, intracellular succinate levels, and succinate dehydrogenase activity in human chondrocytes and cartilage tissue. Cartilage homogenates obtained from 25 patients (20 women, 5 men) and a chondrocyte culture were used. Immunocytochemical analysis revealed SUCNR1 in chondrocyte membranes, while ELISA demonstrated increased levels of both SUCNR1 and succinate in osteoarthritis cartilage, with no notable variations observed between load-bearing and non-load-bearing zones. Succinate dehydrogenase activity remained unchanged. These findings indicate the presence of SUCNR1 in cartilage tissue cells and establish the signaling role of succinate in the pathogenesis of metabolic-phenotype osteoarthritis.
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