FIGURE 3.

Strategic Metabolic Interventions for Renal Protection in SA-AKI. The refined activation of critical metabolic influencers—specifically PGC-1α, AMPK, SIRT1, and PPAR-α—and the enhancement of fatty acid absorption through CD36 mediation offer viable strategies for defending renal integrity amidst sepsis-associated acute kidney injury (SA-AKI). Additionally, strategically modulating PKM2, a key enzyme in the process of aerobic glycolysis, could provide a supplementary pathway to diminish the metabolic imbalances that are hallmark features of SA-AKI. AMPK, adenosine monophosphate kinase; PGC-1α, peroxisome proliferator-activated receptor gamma; Sirt1, sirtuin1; PPAR-α, peroxisome proliferator-activated receptor-α; TFAM, transcription factor A; GLUT, glucose transporter protein; PKM2, pyruvate kinase M2; Glu-6-P glucose 6-phosphate; Fru6-P Fructose 6-phosphate.