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. 2026 Apr 13;16(8):101635. doi: 10.1016/j.jpha.2026.101635

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© 2026 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 10 — Mechanism of diosgenin (DG) action on high-glucose and high-fat (HGHF)-induced human umbilical vein endothelial cells (HUVECs): DG activates the sirtuin 6/nuclear factor erythroid 2-related factor 2 (Sirt6/Nrf2) signaling pathway, reduces reactive oxygen species (ROS) and lipid peroxidation accumulation, and ameliorates mitochondrial dysfunction, thereby inhibiting HGHF-induced ferroptosis in HUVECs and ultimately promoting diabetic wound (DW) healing. Sirt6: sirtuin 6; GSH: glutathione; MDA: malondialdehyde; SLC7A11: solute carrier family 7 member 11; GPX4: glutathione peroxidase 4; CD31: cluster of differentiation 31; VEGF: vascular endothelial growth factor; α-SMA: α-smooth muscle actin.