Podocyte foot process effacement, the hallmark of podocyte injury and proteinuric kidney disease, is often accompanied by the disappearance of these actin filaments. Mundel et al. showed that in differentiated murine podocytes, the actin cytoskeleton was rearranged into fibroblast-like stress fibers ASP1517 HIF inhibitor extending into the processes. It is well established that stress fibers in cultured podocytes correspond to the filamentous actin in podocyte foot processes in vivo and as such represent differentiation of podocytes. Navitoclax adhesion of podocytes to the glomerular basement membrane is mediated by integrin triggered focal adhesions associated to the actin cytoskeleton. The maturation and turn-over of these adhesions is intimately linked to actin-myosin contractility. Interestingly, focal adhesion distribution in podocytes was found to be different as compared to other cell types. Adhesions were located along the entire length of actin stress fibers instead of being restricted to their end, an anatomical precondition for the extensive but dynamically regulated adhesion to the glomerular basement membrane. PAN is a toxic molecule used to induce experimental proteinuria in animals. It alters the stability of the podocyte cytoskeleton associated with the effacement of foot processes, making it a reliable model for glomerular diseases under experimental conditions. In rodents, the strong cytoskeletal damage induced by PAN has been previously shown to be rescued by different pharmaceutical agents. We used this in vitro approach to investigate possible rescue effects of EV. We confirmed the damaging effects of PAN treatment in our in vitro model of differentiated human podocytes. Treatment caused strong morphological and cytoskeletal defects with significant reduction of cell size, a pronounced front-to-back polarized cell shape and significant loss of central actin stress fibers, all elementary processes required for the movement of migratory cells. Consistently, we measured a substantial increase in the migration efficiency of human podocytes similar to previous reports utilizing murine cell systems. In addition to the loss of central actin stress fibers, we detected decreased cell adhesion after PAN treatment accompanied by significant shortening of focal adhesions and their absence in the cell body. These changes in focal adhesion size and adhesion efficiency might be directly linked to the massive defects of the actin cytoskeleton as focal adhesion formation and their turn-over have been associated with cellular tension generated by actin stress fiber contractility.