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Conclusions The antifibrotic effects of GLP-1R activation on pulmonary fibrosis could be attributed to the inhibition of the interaction between NLRP3 inflammasome and PFKFB3-driven glycolysis, and histone lactylation in lung fibroblasts

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However, the FDA mandated a boxed warning stating that the discontinuation of the therapy may result in severe acute exacerbations of hepatitis B and that hepatic function should be monitored closely