Podocytes and their foot processes form an important cellular layer of the glomerular barrier involved in regulating glomerular permeability. Disturbances in podocyte function play a central role in the development of proteinuria in diabetic nephropathy. The retraction of podocyte foot processes forming a slit diaphragm is a common feature of proteinuria. Metformin is an oral antidiabetic agent of the biguanide class that is widely recommended for the treatment of high blood glucose in patients with type 2 diabetes mellitus. In addition to lowering glucose, several recent studies have reported potential beneficial effects of metformin on diabetic kidney function. Furthermore, a key molecule of the antidiabetic mechanism of action of metformin is adenosine 5'-monophospate-activated protein kinase (AMPK), as the metformin-induced activation of AMPK is well documented. The present review summarizes current knowledge on the protective effects of metformin against pathological changes in podocytes that are induced by hyperglycemia.
Keywords: AMP-activated protein kinase; Hyperglycemia; Insulin signaling; Metformin; Podocyte; Reactive oxygen species.
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