Fig. 1 |. lncRNA mechanisms of action.

The figure shows mechanism by which long non-coding RNAs (lncRNAs) have been shown to exert their function in the heart and lead to cardiac hypertrophy. a, Cis or trans regulation. lncRNAs can interact with transcription factors (TFs) to facilitate their activity and promote transcription in cis of a nearby gene (gene X). This lncRNA–TF interaction can also facilitate transcription in trans of a gene at a distant site (gene Y). Alternatively, lncRNA–TF interactions can limit the activity of the TF or the lncRNA could participate in the stabilization of a transcriptional repressor complex, thereby reducing transcription. b, Regulation of alternative splicing. lncRNAs can interact with RNA-binding proteins (RBPs) to facilitate the formation of alternative splice variants. c, Protein interactions. lncRNAs can have a direct influence on the stabilization of the RNA polymerase II (Pol II) complex to promote transcription. Some lncRNAs can also stabilize proteins to facilitate or prolong their activity. d, microRNA (miRNA) sponging by lncRNAs. lncRNAs are also able to interact with and limit the activity of miRNAs. In one mechanism, lncRNAs directly sequester and prevent miRNAs from degrading target mRNAs. In a second mechanism, lncRNAs interact with and suppress the ability of miRNAs to inhibit translation. e, Antisense regulation of mRNAs. lncRNAs can influence the stability of an mRNA through direct interaction and by preventing its degradation. Other mechanisms might exist but remain to be validated in the heart.