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In addition to small-molecule inhibitors like 3PO, activation of the glucagon-like peptide-1 receptor (GLP-1R) has also been shown to attenuate pulmonary fibrosis progression by disrupting NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome/PFKFB3-driven glycolysis and histone lactylation, providing an alternative strategy for targeting PFKFB3-related metabolic reprogramming [26]

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But the Adams DMSA study tells a different story: when demand rises to clear metals, the body steps up glutethione production to meet it in order to clear the detoxed metals from the system

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