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. 2023 Sep 21;20(2):416–436. doi: 10.1080/15548627.2023.2259216

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© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 6. — PRKAA^S496D overexpression attenuates crizotinib-induced cardiotoxicity. AAV9-TNNT2-vector, AAV9-TNNT2-PRKAA^S496D or AAV9-TNNT2-PRKAA^T183D virus was injected into C57BL/6J mice (n = 10). Three weeks after injection, mice were then intragastrically administrated with vehicle or 100 mg/kg crizotinib for another 6 weeks. (A-C) the left ventricular function of mice was measured by echocardiography. (D) heart weight to tibia length ratio (HW: TL). (E) serum was analyzed for CKMB level. n = 5. (F) H&E staining. Scale bar: 40 μm. (G) the gene expression levels relative to Actb in the indicated groups. n ≥ 4. (H, I) Representative Sirius red-stained (upper) and Masson-stained (lower) cardiac sections. Scale bar: 40 μm. (J) TEM observation of the left ventricle from C57BL/6J mice shown in A. (K) the mt-Atp6: Rpl13 ratio was measured as a relative mtDNA level. n = 5. Data were presented as mean ± SD. The P value was calculated by one-way ANOVA with Sidak’s tests (B to D, F, G and K). ****, P < 0.001; ***, P < 0.001; **, P < 0.01; *, P < 0.05; ns, no significance. Crizo: crizotinib.