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. 2022 Sep 14;12:15476. doi: 10.1038/s41598-022-19335-w

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© The Author(s) 2022

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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Aortic remodeling is dependent upon phosphorylation of SMAD3, but not SMAD2 in bicuspid (BAV) and unicuspid (UAV) aortic valve-associated ascending aortic aneurysms. (A) Graph depicting the relationship between elastin breaks and phosphorylated SMAD2 (pSMAD2) in TAV (blue) and BAV/UAV (pink) aortas. (B) Graph depicting the relationship between elastin breaks and phosphorylated SMAD3 (pSMAD3) in TAV (blue) and BAV/UAV (pink) aortas. (C–E) Graphs depicting the level of pSMAD2 (dark grey) and pSMAD3 (light grey) in ascending aortas with mild or severe elastin loss (EL; C), fibrosis (D) and mucoid extracellular matrix accumulation (MEMA; E) in TAV (left) and BAV/UAV (right) aortas. *P < 0.05.