Abstract:

ABSTRACT  Glycogen synthase kinase-3, especialy the glycogen synthase kinase-3β (GSK3β) subtype, has impacted in many life activation, including karyomitosis, cell differentiation, cytoskeletal organization and normal epithelial survival. The patients on long-term Li+ treatment may lead to nephrogenic diabetes insipidus (NDI), indicating that GSK3β might be crucial for urine concentration by the kidneys. Prolonged rapamycin treatment on patients with kidney transplantation leads to an increase in (GSK3β) phosphorylation, accompanied by the reduced expression of slit diaphragm-associated proteins and resulted in an altered cytoskeletal structure and reduced motility of podocytes. GSK3β inhibitors can cause similar effects on padocytes as treatment with rapamycin. GSK3β has been associated with podocytes injury and proteinuria.

Key words: Key word , glycogen synthase kinase-3β, nephrogenic diabetes insipidus, podocytes injury, , Li+, rapamycin