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The inactivation of GLP-1 and GIP by DPP-4 in consequence leads to diminished binding of ligands of the chemokine receptor CXCL-12 to chemokine receptors CXCR4 and CXCR7 [28]

Similar to RSL3induced ferroptosis, such cell death can be rescued with DFOM (an iron chelator), U0126 (a MEK inhibitor), and vitamin E (an antioxidant) 2, suggesting that GPx4 activity inhibition is a major contributor to ferroptosis

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PMCID: PMC11642516

This review will explore how GLP-1R signaling could inhibit interdependent inflammation in both the lung and nervous system

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