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It may be relevant for studies examining cellular aging, structural protein turnover, and oxidative signaling pathways under controlled conditions

GLP-1R activation exerted antifibrotic effects by blocking the interaction between the NLPR3 inflammasome and PFKFB3-driven glycolysis, leading to the inhibition of lactate production and subsequent histone lactylation, and thereby decreasing profibrotic gene expression in fibroblasts under inflammatory stress

Signaling mechanisms leading to the regulation of differentiation and apoptosis of articular chondrocytes by insulin-like growth factor-1

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