Figure 1.
Endothelial-podocyte crosstalk. (A) Transmission electron micrograph of a normal mouse glomerular filtration barrier shows podocyte (P) foot process, glomerular basement membrane (GBM), and endothelial cells (EC; scale bar: 500 nm). (B) Under physiologic conditions (left), various secreted factors are exchanged between podocytes and endothelial cells to allow for maintenance of the glomerular filtration barrier. During diabetic nephropathy (right), increased reactive oxygen species (ROS) production can lead to thinning of the glycocalyx of the endothelium, as well as cellular damage to both endothelial cells and podocytes. Overactivation of several pathways leads to endothelial dysfunction, podocyte foot effacement, and eventually podocyte detachment. Abbreviations: eNOS, endothelial nitric oxide synthase; ETAR, endothelin A receptor; TGFβ, transforming growth factor β; TRPC6, transient receptor potential canonical 6.