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. Author manuscript; available in PMC: 2024 Nov 1.
Published in final edited form as: Nat Rev Cardiol. 2023 Nov 20;21(5):326–345. doi: 10.1038/s41569-023-00952-5

Fig. 3 |. lncRNA regulation of miRNA-dependent cardiac hypertrophy.

Fig. 3 |

Long non-coding RNAs (lncRNAs), such as CHRF (cardiac hypertrophy related factor) and XIST (X-inactive specific transcript), sequester microRNAs (miRNAs) and prevent their binding to target mRNAs. Myeloid differentiation primary response 88 (MYD88) has been shown to promote inflammatory signalling and lead to cardiac hypertrophy after myocardial infarction. miR-489 suppresses MYD88 activity. Given that CHRF acts as an endogenous sponge of miR-489 and downregulates miR-489 expression levels, CHRF releases MYD88 from the inhibitory influence of this miRNA, enabling the downstream cardiac hypertrophic response. Similarly, the Toll-like receptor 2 (TLR2) is essential for activating the IGF1–PI3K–AKT pathway and promoting cardiac hypertrophy. miR-101 directly targets TLR2 to repress its activity. By suppressing the action of miR-101, the lncRNA XIST activates the TLR2-dependent cardiac hypertrophic response.