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. 2023 Nov 30;13:220. doi: 10.1186/s13578-023-01168-3

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Analysis of the differentially expressed genes in samples from heart failure patients. A 2D visualization of GSTT2, GSTZ1 and GSTM2 gene expression in the LV and LA. B Analysis of GSTT2, GSTZ1 and GSTM2 protein abundances according to proteomics. C Immunofluorescence analysis of GSTM2 (red) expression in cardiomyocytes (stained with the cardiomyocyte marker α-actinin, green) from clinical human cardiac hypertrophy (CH) tissues and normal heart tissues. The nuclei were stained with DAPI (blue). Scale bar: 200 μm. D Immunofluorescence analysis of GSTM2 (red) expression in cardiomyocytes (stained with the cardiomyocyte marker α-actinin, green) from the heart tissues of sham or TAC model mice. The nuclei were stained with DAPI (blue). Scale bar: 100 μm. E Representative Masson staining results to assess fibrosis in heart tissues from mice injected with AAV9-GSTM2 or control AAV9 via the tail vein for 3 weeks, then subjected to TAC, and analyzed 4 weeks later. F Statistical analysis of the heart weight (HW)/body weight (BW) ratios of mice subjected to TAC surgery 4 weeks after surgery (n = 6 mice per group; *p < 0.05 versus sham group). G Assessment of left ventricular end-diastolic diameter (LVEDd) in mice, n = 6. ^*p < 0.05