Abstract
Diabetic kidney disease (DKD) is the most common diabetic complication and is a leading cause of end-stage kidney disease. Increasing evidence shows that DKD is regulated not only by many classical signaling pathways but also by epigenetic mechanisms involving chromatin histone modifications, DNA methylation, and non-coding RNA (ncRNAs). In this review, we focus on our current understanding of the role and mechanisms of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the pathogenesis of DKD. Of them, the regulatory role of TGF-β/Smad3-dependent miRNAs and lncRNAs in DKD is highlighted. Importantly, miRNAs and lncRNAs as biomarkers and therapeutic targets for DKD are also described, and the perspective of ncRNAs as a novel therapeutic approach for combating diabetic nephropathy is also discussed.
Highlights
Diabetic kidney disease (DKD) is one of the most predominant diabetic complications and is a leading cause of chronic kidney disease (CKD)
By direct interaction with miRNAs or inflammatory molecules, long non-coding RNAs (lncRNAs) play as sponges, inhibitors, or activators to influence either fibrogenesis or inflammatory response. All these findings have demonstrated a critical role of lncRNAs therapeutic targets in the pathogenesis of DKD
Arid2-IR is regulated by Smad3, knockdown of Arid2-IR in tubular epithelial cells (TECs) has no effect on transforming growth factor β (TGF-β)/Smad-mediated fibrosis but promotes IL-1β-induced NF-κB-driven renal inflammation in obstructive kidney disease (Zhou et al, 2015)
Summary
Diabetic kidney disease (DKD) is one of the most predominant diabetic complications and is a leading cause of chronic kidney disease (CKD). The mechanisms of ncRNAs on renal fibrosis and inflammation in DKD based on the TGF-β/Smad-mediated signaling pathway will be discussed. A high level of miR-23a was observed in diabetic patients and HG-cultured TECs. It directly targets the nuclear transcription co-repressor Ski-related novel protein N (SnoN) (Tan et al, 2006), a crucial negative regulator to TGFβ/Smad3-mediated signaling pathway, to induce fibrosis in DKD (Xu et al, 2018a).
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