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. 2020 Mar 24;8:187. doi: 10.3389/fcell.2020.00187

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Copyright © 2020 Zhao, Zou and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Simplified schematic diagram of pathological role of TGF-β1 signaling in diabetic kidney disease. Pathogenic stimuli in diabetic kidney disease like hyperglycemia, angiotensin-II, reactive oxygen species, mechanical stretch, advanced glycation end products, and thrombospondin-1 are able to active TGF-β1 signaling. TGF-β1 signaling plays an important role in mediating renal fibrosis, inflammation, and autophagy in proximal tubular epithelial cells in diabetic kidney disease. TGF-β, transforming growth factor-beta; ROS, reactive oxygen species; PTECs, proximal tubular epithelial cells; AGE, advanced glycation end products; TSP-1, thrombospondin-1; ECM, extracellular matrix.