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. 2016 Sep 30;7:12864. doi: 10.1038/ncomms12864

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(a) Proposed model for the initiation of the early stages of DN through lnc-MGC, the miR-379 megacluster and related ER stress. Diabetic conditions and ensuing increases in TGF-β1 can promote ER stress and induce lnc-MGC via Smad2/3 and CHOP. This results in increased expression of nearly 40 megacluster component miRNAs and subsequent downregulation of numerous targets whose functions are related to hypertrophy, ECM production and fibrosis associated with early features of DN. Targeting lnc-MGC in vivo with specific LNA GapmeRs can attenuate these pathological events, and thereby prevent further disease progression. Please see main text for additional details. (b) A schematic model of CHOP upregulation through two pathways: first, XBP-1 splicing activated by ER stress; and second, reduction in levels of ATF3 (a repressor of CHOP) due to targeting by the cluster miR-494 in MC treated with TM, HG or TGF-β1. CHOP in turn can induce lnc-MGC and ER stress in positive feedback loops.