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. 2023 Jan 31;44(7):1366–1379. doi: 10.1038/s41401-023-01057-y

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© The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Fig. 8 — a The time course of AAV9-mediated TAK1 overexpression. Recombinant AAV9 vectors harboring TAK1 or GFP with a c-TnT promoter [3 × 10¹¹ vector genomes/mouse] were injected into the tail veins of the mice 5 weeks before MI/R. b, c Representative infarct images obtained by Evans blue/TTC staining in each group. d Cardiac troponin-I (cTnI) levels in plasma 4 h after perfusion. e Cardiac creatine kinase-MB (CK-MB) levels in plasma 4 h after perfusion. f, g Western blot images and quantitative analysis of p-TAK1, TAK1, p-p38, p38, p-JNK, JNK, Bcl-2 and Bax protein expression in ischemic myocardial tissue. The data are shown as the mean ± SEM (n = 6 for each group). ^#P < 0.05 and ^##P < 0.01 vs. the MI/R + AAV9-cTnT-GFP group. ^$P < 0.05 and ^$$P < 0.01 vs. the MI/R + AAV9-cTnT-GFP + NG-R1 group.