Cellular and molecular mechanism actions of steroids on kidney cells
Nephrotic syndrome (NS) is common kidney disorder characterized by proteinuria and edema. Steroids are generally used in the treatment of NS; however, their mechanism of action is not fully understood. Evidence shows that podocytes, specialized kidney cells, are the center of pathophysiology and targets of therapy in NS. The PubMed database was searched for English language articles focusing on the steroids effects on podocytes. Steroids therapy can directly target the podocytes and regulate their morphology and function after injury. Beyond anti-inflammatory properties, steroids exert antiproteinuric effects on podocytes. The mechanisms by which steroids exert their renoprotective effect are mediated by direct functioning on podocytes; promoting actin filament stabilization, and decreasing the reactive oxygen species (ROS) production. Moreover, steroids protect podocytes from injury and apoptosis by elevating the Bcl-xL expressions, decreasing the p53, p21 and Bax, and restoring antiapoptotic signaling; leading to prolonged podocyte survival. Understanding the cellular and molecular mechanisms of steroids on kidney cells would promise an optimum therapeutic benefit of steroid therapy.