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. 2024 Apr 9;83(9):1156–1168. doi: 10.1136/ard-2023-225158

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© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ on behalf of EULAR.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Comparison of differentially expressed genes (DEGs) in allogeneically transplanted mice treated with mCAN10 or nintedanib. (A) Principal component analysis depicting the distribution of various sample groups. (B) Intersection of DEGs between nintedanib-treated mice (Nin_DEGs) and mCAN10-treated mice (mCAN10_DEGs), using a p-adjusted value cut-off of ≤0.05 and a |log₂ fold change| cut-off of ≥1. (C) The number of overlapping biological process-related terms between mCAN10 and nintedanib treatment. (D) Comparison plot illustrating the signature signalling pathways between nintedanib and mCAN10 treatments. ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; MAP, mitogen-activated protein.