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. 2021 Sep 12;116(1):51. doi: 10.1007/s00395-021-00891-7

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 11 — Proposed mechanisms of pulmonary vascular dysfunction in DM + HC + CKD. Upper cells represent endothelial cells, lower cells the smooth muscle cells. Significant differences in DM + HC + CKD compared to Healthy are shown as highlighted numbers in the figure. AKT protein kinase B, Big-ET-1 big endothelin 1, Ca²⁺ calcium, cGMP cyclic guanosine monophosphate, CM calmodulin, ECE endothelin converting enzyme, ET-1 endothelin 1, ET_A endothelin receptor A, ET_B endothelin receptor B, GTP guanosine triphosphate, Gq G alpha subunit, IP3 inositol triphosphate, L-Arg l-arginine, M-A myosin–actin, MLCk myosin light chain kinase, MLCp myosin light chain phosphatase, NO nitric oxide, NOS nitric oxide synthase, PDE5 phosphodiesterase 5, PIP3 phosphatidylinositol triphosphate, PKG protein kinase G, PLC phospholipase C, sGc soluble guanylate cyclase, SMC smooth muscle cell, VASP vasodilatation stimulating proteins. This figure is produced by adapting images from Servier Medical Art by Servier (https://smart.servier.com/), licensed under a Creative Commons attribution 3.0 Unported Licence