Figure 9.

Schematic illustration of the mechanism for p-Tau to mediate METH-induced podocyte pathology. Upon METH treatment, the activated GSK3β (phosphorylated GSK3β) could lead to Tau phosphorylation. The phosphorylated Tau may trigger podocyte pathology including podocyte simplification, foot process effacement, and podocyte specific protein loss. Inhibiting GSK3β activation by LiCl could alleviate the podocyte injury induced by METH. The luteolin could prevent the podocyte pathology, and it might be p-Tau dependent.