Figure 1

Schematic diagram of the effects and underlying mechanisms of lncRNAs in various fibroses. Green: LncRNAs involved in liver fibrosis. APTR promotes HSC activation via recruitment of the PRC2 complex to and subsequent inhibition of the p21 promoter. The inhibited expression of the tumor repressor gene p21 promotes ECM synthesis and liver fibrosis. LincRNA-p21 also promotes liver fibrosis via a direct decrease in p21 expression. MEG3 inhibits cell proliferation and induces apoptosis, but TGF-β1 decreases MEG3 expression via mediation of the methylation of the MEG3 promoter, which induces liver fibrosis. MiRNA-222 is involved in liver fibrosis via targeting of the GAS5 gene. However, GAS5 is a competing endogenous RNA (ceRNA) that directly binds to miR-222 and increases the level of the tumor suppressor p27, which inhibits HSC activation and proliferation. GAS5 is downregulated in activated HSCs and fibrotic liver tissues. Yellow: LncRNAs involved in cardiac fibrosis. TGF-β1-induced upregulation of lncRNA H19 correlates with a gradual decrease in DUSP5 expression, which represses the DUSP5/ERK1/2 signaling pathway in primary rat cardiac fibroblasts. Ang II treatment decreases the levels of lncRNA-NR024118 and Cdkn1c in cardiac fibroblasts via its cognate receptor, Ang II receptor type I (AT1). MIAT functions as a ceRNA for miR-24 and upregulates TGF-β1 expression to induce the subsequent activation of CFs. Blue: LncRNAs involved in kidney fibrosis. H19 is upregulated in TGF-β2-induced HK-2 cell fibrosis via sponging of miR-17 (artificial miRNA decoy), and np_5318/np_17856 level is upregulated in TGF-β-induced cells, which promotes the fibrotic process. CYP4B1-PS1-001/ ENSMUST0000 0147869 is downregulated in kidney tissues from db/db mice and promotes the proliferation of MCs. Brown: LncRNAs involved in lung fibrosis. MRAK088388 may be regulated in lung myofibroblast growth and collagen deposition via sponging of miR-29, which binds to N4bp2. MRAK081523 may compete with the let-7i pool to regulate the expression of Plxna4. MiR-489 may function as an anti-fibrotic miRNA via targeting MyD88 and Smad3, and the lncRNA CHRF inhibits miR-489 expression. Upregulated uc.77 and 27000086A05Rik target Zeb2 and Hoxa3, respectively. Downexpression of BGas induces CFTR overexpression and results in LEC proliferation and ECM production. ‘T’ (blunt) ends of connectors represent negative regulation, and pointed (arrowhead) ends represent positive regulation. Red-colored bold font indicates lncRNAs. CFs, cardiac fibroblasts; ECM, extracellular matrix; HSCs, hepatic stellate cells; LECs, lung epithelial cells; MCs, mesangial cells.