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. 2022 Mar 3;28:27. doi: 10.1186/s10020-022-00455-y

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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 — Molecular hydrogen alleviates the hyperpermeability of the vascular endothelium in ALI. The interendothelial junctions of ECs include tight junctions and adherens junctions. Occludin and claudins are linked to the zonula occludens. The cytoplasmic domain of VE-cadherin binds to α-catenin and β-catenin to firmly maintain EC–EC junctions. RhoA activates Rho kinases and myosin light chain kinase, which phosphorylates the myosin light chain, inducing actomyosin contractility and weakening endothelial cell–cell adhesion. Molecular hydrogen could increase the expression of VE-cadherin and occludin. It also inhibits the expression of RhoA, reduces the expression of ICAM-1 and its release from the cell, and inhibits the adhesion of monocytes to ECs