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Preclinical signals regarding potential effects on thyroid C-cells (observed with GLP-1 agonists as a class), as well as theoretical questions about bone metabolism and cardiovascular function, are being monitored in ongoing trials
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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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