Figure 9.

Proximal tubular B⁰AT1 is important for the physiology of renal glucose and albumin retention (left) but potentially deleterious in aristolochic acid (AA)-induced nephropathy (right). The former may be due to structural or functional interactions of transport proteins colocalized to the brush border of the early proximal tubule. The latter may involve promotion of p16-mediated senescence that is facilitated by the uptake of neutral amino acids (aa⁰) via B⁰AT1, including glycin and branched-chain amino acids (BCAAs). Blue text and arrows refer to effects related to B⁰AT1 function. “?” indicates hypothetical changes/pathways. See discussion for more details. aa⁺, cationic amino acid; Ccl2, C-C motif chemokine ligand 2; Col1a1, collagen type I-α₁; GLP-1, glucagon-like peptide-1; KIM-1, kidney injury molecule-1; MAP17, 17-kDa membrane-associated protein; mTORC1, mammalian target of rapamycin complex 1; OAT, organic anion transporter; SGLT2, Na⁺-glucose cotransporter 2.