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. 2019 Nov 29;9:17897. doi: 10.1038/s41598-019-52872-5

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed model for ischemic-hypoxia mediated podocyte injury. Ischemia-stroke rats develop systemic hypoxia that induces HIF1α accumulation in several susceptible sites including glomerular podocytes. HIF1α drives ZEB2 expression, which in turn induces TRPC6 expression. Elevated TRPC6 increases intracellular calcium levels and calcium-dependent phosphorylation of FAK elicits cytoskeletal rearrangements. These cytoskeletal rearrangements eventually manifest in the effacement of podocyte foot-processes and increased permeability to proteins and large molecules. The overactivity of the HIF1α/ZEB2/TRPC6 axis in podocytes elicits cytoskeletal abnormalities and proteinuria.