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GLP-1R activation exerted antifibrotic effects by disrupting the interaction between the NLRP3 inflammasome and PFKFB3-driven glycolysis, and subsequently inhibiting lactate-mediated histone lactylation to reduce the expression of profibrotic genes in activated lung fibroblasts (Fig
In terms of safety and tolerability of the compound, there were fewer adverse events per 100 patients across all experimental groups administered cagrilintide
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