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. 2022 Mar 11;72:7. doi: 10.1186/s12576-022-00829-1

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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. 3 — Defective autophagy in VSMCs increases passive arterial stiffness at high pressures. Aortic stiffness, E_p, for Atg7^+/+ SM22α-Cre⁺ (+/+ , open symbols) and Atg7^F/F SM22α-Cre⁺ (F/F, closed symbols) animals was determined at 80–120 (N) and 100–140 (H) mmHg in the presence of extracellular Ca²⁺ (a). Absolute change of E_p by removal of extracellular Ca²⁺ (b) at physiological (N) and high (H) pressures. Two-way ANOVA with pressure and genotype effect indicated and with Sidak’s multiple comparisons post-test. *p < 0.05 **p < 0.01 (n = 7)