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. 2023 Aug 17;24:202. doi: 10.1186/s12931-023-02501-7

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© The Author(s) 2023

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Changes of pulmonary vascular medial wall thickness and RV lesions in SuHx rats. (A) Representative photomicrographs of hematoxylin and eosin (H&E) stain of pulmonary vessel cross sections, H&E stained and masson’s trichrome stain of RV sections. (B, C) Scatter dot plot showing the comparison of vessel wall thickness and vessel wall area of vessels (outside diameter > 50 μm) between the CTL and SuHx groups. (D, E) Scatter dot plot showing the comparison of cross-sectional area of right ventricle cardiomyocyte and fibrosis between two groups. Data were presented as mean ± S.E.M., control group n = 5–7, SuHx group n = 6–7, *P < 0.05, **P < 0.01, compared with the control group. W: week