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. 2022 Jan 10;13(1):38. doi: 10.1038/s41419-021-04484-z

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — A GSEA analysis revealed a positive correlation between METTL14 and ncRNA processing and degradation. B A significant negative association was identified between METTL14 mRNA and TINCR expression. C HG treatment of cardiomyocytes significantly increased TINCR expression, **P < 0.01, ***P < 0.001. D. TINCR was significantly upregulated in DCM rats in contrast to controlled rats, **P < 0.01. E, F qRT-PCR showed that silence of METTL14 (E) upregulated, while overexpression of METTL14 (F) suppressed TINCR expression in cardiomyocytes, **P < 0.01. G, H Cardiac function analysis (G), electron microscopy imaging (H) showed that injection of METTL14 dramatically reversed the myocardial damage caused by DCM, however, co-expression of TINCR abrogated the METTL14-mediated influence, *P < 0.05, **P < 0.01. I The expressions of pyroptosis-related proteins was detected in H9c2 and NRVMs cells upon indicated treatments.