Fig. 8: Schematic diagram of FGF21-mediated enhancement of endothelium-dependent relaxation. | Cell Death & Disease

Fig. 8: Schematic diagram of FGF21-mediated enhancement of endothelium-dependent relaxation.

From: Fibroblast growth factor 21 Ameliorates diabetes-induced endothelial dysfunction in mouse aorta via activation of the CaMKK2/AMPKα signaling pathway

Fig. 8: Schematic diagram of FGF21-mediated enhancement of endothelium-dependent relaxation.

The normal function of vascular endothelial cell is impaired by oxidative stress that is initiated by metabolic disorders. FGF21 binds to FGFRs (i.e., FGFR1) to potentiate CaMKK2 and AMPKα activities. On the one hand, AMPKα upregulates the expressions of CAT, Nrf-2 and HO-1 to abrogate oxidative stress. On the other hand, AMPKα directly enhances the activity of eNOS. The strengthened eNOS activity leads to an increased production of nitric oxide and restoration of endothelium-dependent vasodilatation

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