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. 2015 Jun 4;13:181. doi: 10.1186/s12967-015-0538-5

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© Masola et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Involvement of HPSE in renal fibrosis. Several factors (high glucose concentrations, ROS, AGE) can increase HPSE production in both glomerular and tubular cells. The same factors induce cathepsin-l production by renal tubular cells, and this activates HPSE. Then the active HPSE can sustain inflammation by activating macrophages recruited from the circulation. During stress conditions both tubular and inflammatory cells release FGF-2 and TGF-β that, thanks to the higher amounts of HPSE, may activate the intracellular machinery leading to EMT.