Podocytes are injured in many forms of human and experimental glomerular disease such as focal segmental glomelurosclerosis, diabetic nephropathy, and crescentic glomerulonephritis. The singularity of the actin cytoskeleton in podocytes and its critical role for podocyte function is well known.
Indeed, podocytes express unique actin-associated proteins such as synaptopodin, mutation or absence of alfa-actinin-4 result in glomerulosclerosis due to podocyte loss by unknown reasons, and several stimuli like polycations and mechanical stress are known to induce rapid and profound reorganization of the actin cytoskeleton in podocytes.
Since it was shown that palladin is expressed and localized to various actin structures in podocytes, that palladin induces and is required for stress fiber formation, and that palladin is known to interact with several proteins expressed in podocytes (alfa-actinin, VASP and ezrin), it seems that palladin plays an important role for the organization of the actin cytoskeleton in podocytes.
Elucidation of the role of palladin and its binding partners in podocytes as well as elucidation of its implication in renal disease will provide new insights into glomerular diseases and new perspectives in therapeutics.
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