Fig. 8 | Scientific Reports

Fig. 8

From: SGLT2 inhibition mitigates transition from acute kidney injury to chronic kidney disease by suppressing ferroptosis

Fig. 8

Schematic diagram of the therapeutic effect of luseogliflozin, showing how it effectively reduces I/R injury and prevents fibrosis in mice. Under normal conditions, I/R injury reduces tubular mitochondrial function and increases oxidative stress. In addition, tubular metabolism shifts from fatty acid oxidation to glycolysis, resulting in accumulation of polyunsaturated fatty acids (PUFAs) and leading to lipid peroxidation and tubular ferroptosis. Next, macrophage infiltration and inflammatory cytokine production occur, leading to tubular fibrosis and the transition from acute kidney injury (AKI) to chronic kidney disease (CKD). Sodium-glucose cotransporter 2 (SGLT2) inhibitors increase the starvation regulator Sirtuin-3 (Sirt3) and also show a tendency to increase pAMPK. Mitochondrial function is improved, oxidative stress is lowered, and PUFA accumulation is prevented by inhibiting the tubular metabolic shift from fatty acid oxidation to the glycolytic system. Consequently, ferroptosis and development of the AKI to CKD transition are prevented.

Back to article page