Fig. 2.

Function of LncRNAs in diabetes-related renal inflammation and fibrosis. LncRNAs can regulate the expression of adjacent and distal genes by various biological mechanisms in DKD. As shown above, a LncRNAs promote the binding of H3K4me3 or H3K27me3 to the gene promoter to affect its expression via recruiting chromatin remodeling complexes such as PRC2 and MLL1. LncRNAs bind transcription factors or cofactors to affect the transcription of target genes as scaffolds: b LncRNAs regulate NLRP3 inflammasome signaling pathway by interacting with p50, the subunit of NF-κB; c LncRNA MALAT1 accelerates β-catenin nuclear accumulation through physical binding to SRSF1, and thus feedback to promote the expression of LncRNA MALAT1 and contribute to renal fibrosis; d LncRNAs also act as regulators of inflammation via directly interaction with Egr-1. In addition, e LncRNAs located in the cell cytoplasm regulate gene expression by acting as molecular sponges and competitively binding to miRNA. EED, embryonic ectoderm development; PRC2, polycomb repressive complex 2; SUZ12, PRC2 subunit; MLL1, mixed-lineage leukemia 1; Egr‐1, early growth response protein 1