FIGURE 2.

Metabolic Shift in Tubular Epithelial Cells During Septic Acute Kidney Injury. At the advent of SA-AKI, renal tubular epithelial cells (TECs) experience a profound metabolic transformation, migrating from OXPHOS toward a predominance of aerobic glycolysis. Within this metabolic realignment, the bulk of pyruvate forged by glycolytic processes eschews mitochondrial entry, opting instead for conversion into lactate—a process catalyzed by lactate dehydrogenase (LDH). This strategic metabolic adaptation is key, supporting an increased production of ATP through glycolysis to meet the amplified energy requirements imposed by the septic challenge. GLUT, glucose transporter protein; PFKFB3, fructose-2,6-bisphosphatase 3; HK2, hexokinase 2; PKM2, pyruvate kinase M2; Glu-6-P glucose 6-phosphate; Fru6-P Fructose 6-phosphate; LDH, Lactate Dehydrogenase; MCT, Monocarboxylate TransporterCD36, cluster of differentiation 36; TCA, tricarboxylic acid cycle; FADH2, reduced flavin adenine dinucleotide; NADH, reduced nicotinamide adenine dinucleotide; ATP, adenosine triphosphate; ADP, adenosine diphosphate.