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When the oxidative stress state persists and the damage progresses, senescent cells enter a senescent state marked by p16 upregulation, which consequently inhibits the kinases CDK4 and CDK6, thereby maintaining the stagnant state of the cell cycle [133, 134]

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Being the proximal tubule a major target for many nephrotoxicants, it is logical that cell-based in vitro models that seek to resemble this segment of the nephron should be characterized by the expression of important markers, including SLC22A6 (OAT1), SLC22A8 (OAT3), SLC22A2 (OCT2) on the basolateral membrane and ABCB1 (P-gp), SLC47A1 (MATE1), SLC47A2 (MATE2), ABCC2 (MRP2), ABCC4 (MRP4), ABCG2 (BCRP), and the endocytosis receptors megalin and cubilin on the apical membrane (Bajaj et al