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. 2025 Aug 11;16:1550925. doi: 10.3389/fendo.2025.1550925

Figure 7.

High glucose environment promotes the production of reactive oxygen species (ROS), leading to increased activation of neutrophils and NETosis. This upregulates CXCL8 and CXCR2, which activates macrophages (MPs), contributing to kidney injury.

Hypothesized mechanism of the progression of kidney damage in patients with T2DM and T2DKD. This schematic diagram illustrates the proposed hypothesis. In patients with T2DM and T2DKD, prolonged hyperglycemia results in elevated ROS levels, promoting kidney damage. This triggers inflammatory responses, leading to neutrophil aggregation and increased NET formation, which subsequently activate MPs through CXCL8 and CXCR2 interactions. Altered neutrophil and MP levels and functions further intensify inflammation, exacerbating kidney damage.