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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. 7 — A Western blot experiment was performed to test the expression of pyroptosis-related proteins in cardiomyocytes treated with Lv-TINCR and MCC950. B RNA pulldown using specific TINCR probe revealed a direct interaction between TINCR and NLRP3. C Cells were treated with ActD, then existing NLRP3 mRNA was detected at different time point. Silence of TINCR significantly decreased NLRP3 stability, P < 0.001. D METTL14 suppressed NLRP3 stability, while co-transfection of Lv-TINCR partially reversed this effect, *P < 0.05, **P < 0.01. E A scheme of the proposed mechanisms: TINCR was modified by METTL14-mediated m6A methylation, which induced suppression of TINCR in cardiomyocytes. Suppressed TINCR caused decreased stability of NLRP3 and thereby induced its downregulation. Eventually, downregulated NLRP3 inhibited pyroptosis and DCM progression.