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. 2020 Feb 24;11(2):146. doi: 10.1038/s41419-020-2337-z

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© The Author(s) 2020

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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Fig. 8 — Kidney disease, TGF-β, and other injury factors result in combined actions of S100A16, Myh9, and Ca²⁺ in injured epithelial cells. The EMT and cytoskeleton reorganization lead to the transition of renal epithelial cells into myofibroblasts, followed by accumulation of extracellular matrix and aggravation of renal tubulointerstitial fibrosis.