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. 2012 Feb;5(1):17–27. doi: 10.1093/ckj/sfs001

Fig. 1.

Fig. 1.

Proposed interactions of endothelin (ET-1) with the glomerular basement membrane (GBM) of the glomerular capillary, its endothelial cells (GEC) and podocytes/slit diaphragm. ET-1 is produced by cells on both sides of the GBM, namely GEC and podocytes. ET-1 is released from GEC and may interact either directly with GBM (1) the slit diaphragm (2) or the podocyte, also in the reverse direction (3). Podocyte-derived ET-1 (4) may also affect the GBM and vice versa. ET-1 activates podocyte endothelin ETA receptors (ETA R) activating mitogen-activated protein kinases (MAPKs) p38 and p44/p42 (5), growth promoters (p21waf/cip1), or inflammation (NF-kappaB) (6). ET-1 also causes disruption of the podocyte F-actin cytoskeleton (7) and slit diaphragm dysfunction via activation of rho kinase and PI3-kinase. Figure reproduced from reference [11] with permission of the publisher.