Peter Mundel, a well-known researcher of podocyte biology, gave our Renal Grand Rounds today. Here's what I took away from this morning's talk:-regulation of the podocyte's actin cytoskeleton is postulated to be the final common pathway in most instances of nephrotic syndrome/proteinuria.
-in some ways it is better to think of the podocyte as a modified smooth muscle cell rather than a modified epithelial cell based on its intricate network of actin & myosin which mediate contractility.
-the medication cyclosporine (used in the treatment of some refractory forms of nephrotic syndrome) acts NOT on modulation of immune cell function as previously assumed, but rather on direct effects on the podocyte actin cytoskeleton, as detailed in a prior post.
-a key event in generating abnormal, protein-leaking podocytes is turning them from a stationary cell to a motile one. This key transition is mediated by three distinct Rho GTPase proteins, already established to mediate motility in several cell types. In general, Cdc42 and Rac1 promote podocyte motility, whereas RhoA promotes podocyte stabilization. It is possible that targeting these Rho GTPase pathways could lead to novel therapies for podocytopathies, and this is being investigated.
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