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. 2020 Jul 27;117(6):1532–1545. doi: 10.1093/cvr/cvaa233

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© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Genes induced in pathological CMs are increased in stressed human iPS-derived CMs. (A) Representative images of hiPS-CMs in control conditions or after NE and AngII treatment. Immunofluorescence for cardiac troponin T (cTnT) and nuclei DAPI. (B) Calcium transient analysis of the frequency of spontaneous calcium transients and (C) calcium transient analysis of the calcium release of control (C) or NE/Ang II treated (Stress) CMs. (D) Representative spontaneous calcium transients in control (upper panel) and stressed (lower panel) iPS-derived CMs. (E) Human NT-proBNP content in the supernatant of control and NE/AngII (stress) treated CMs determined by ELISA assay (n = 5). (F) Real-time PCR analysis of stress markers and the newly identified genes on NE-AngII treated CMs. Data are expressed as mean fold change ± SEM; *P < 0.05 compared to control (C) with unpaired t-test (n = 3–9) or in a two-way ANOVA.