Figure 2.

Disturbed cellular metabolism of T cell: pathogenesis of certain kidney disease. In the progression of certain kidney diseases, T cell metabolism undergoes a series of changes to provide necessary energy support. Targeting T cell metabolism is expected to offer new therapeutic options for kidney disease treatment. OXPHOS, oxidative phosphorylation; FAO, fatty acid oxidation; F-6-P, fructose-6-phosphate; F-1,6-P, glucose-6-phosphate; G-6-P, glucose-1-6-bisphosphate; Glc, glucose; GLUT, glucose transporters; OPA1, optic atrophy 1; LKB1, liver kinase B1; CAMK, calcium/calmodulin-dependent protein kinase; PFKP, 6-phosphofructokinase, platelet type; NAMPT, nicotinamide phosphoribosyltransferase; NMN, nicotinamide mononucleotide; NAM, nicotinamide; TIGIT, T-cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif domain; eIF5A, translation elongation factor eukaryotic translation initiation factor 5A; FABP, fatty-acid-binding proteins; SGLT2, sodium-glucose co-transporter 2.