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. 2021 Apr 29;12:647650. doi: 10.3389/fphar.2021.647650

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Copyright © 2021 Huang, Zhang and Ge.

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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Schematic diagram for the functions and mechanism of lncRNA MALAT1 in regulating renal fibrosis in diabetic rats. MALAT1 is induced by high glucose in renal tubular epithelial cells in vitro and in renal tubular epithelium in STZ-diabetic rats in vivo, which sponges miR-2355-3p and positively regulates expression of IL6ST gene. IL6ST is an identified regulator to phosphorylate STAT3 and activates its downstream master pro-inflammatory transcription factor NF-kB. Then, NF-kB transcriptionally upregulates the fibrogenic marker genes, including LN, FN, coi I, and col IV, as well as secretion of pro-inflammatory cytokines IL-6 and TNF-α, thus promoting renal fibrosis in diabetic rats.