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. 2022 Feb 11;72:2. doi: 10.1186/s12576-022-00826-4

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© The Author(s) 2022

Open AccessThis 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. 7 — This scheme illustrates the proposed role of β-AR/Gsα/AC5 signaling in the heart of BO mice. β-AR/Gsα/AC5 signaling is activated by the BO treatment, leading to oxidative stress via activation of NOX4/ASK1/p38 and phosphorylation of CaMKII (Thr-286), which mediates PLN phosphorylation at Thr-17. In addition, cAMP derived from AC5 mediates oxidative stress and PLN phosphorylation at Ser-16. These changes might cause fibrosis, myocyte apoptosis and oxidative stress in the heart of BO mice, leading to cardiac dysfunction