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. 2022 Jan 1;15(1):38–48. doi: 10.1007/s12265-021-10147-3

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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 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/.

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Fig. 3 — Inflammation and cardiac function markers in SARS-CoV-2-infected normotensive and hypertensive hACE2 transgenic mice with or without AT1R blocker treatment. a, b Western blots of inflammation markers, IL-6 and TNFα, analyzed by ImageJ. c mRNA expression of inflammation markers quantified by qRT-PCR in control (normotensive hACE2 transgenic mice) and hypertensive hACE2 transgenic mice without and with AT1R blocker treatment. d Ang II/Ang1-7 imbalance as a key player in cardiac injury. e Western blots of cardiac MasR and GAPDH analyzed by ImageJ; f serum levels of Ang II, Ang 1-7, cardiac troponin I (cTnI), and creatine kinase-MB(CK-MB) in control normotensive hACE transgenic mice and hypertensive hACE2 transgenic mice without or with AT1R blocker treatment (n=3/group, *P<0.01 vs. control, #P<0.05 vs. untreated hypertensive hACE2 transgenic mice), Wilcoxon rank. Immunoblots (a and e) are representatives of three independent experiments.