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. 2022 Sep 5;7:309. doi: 10.1038/s41392-022-01160-2

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Protective effect of genistein on Δ9-THC-induced endothelial dysfunction in atherosclerosis. a △9-THC binds and activates the CB1R signaling, which activation causes inflammation and oxidative stress leading to endothelial dysfunctions in atherosclerosis through inducing PKA, p38 MAPK and NF-κB signaling pathways. b CB1R antagonist genistein alleviates the △9-THC-induced deleterious effects in endothelial cells, which suggest that genistein has promising therapeutic potential