Cannabinoid receptor 1 antagonist genistein attenuates marijuana-induced vascular inflammation

Abstract

(Cell 185, 1676–1693.e1–e23; May 12, 2022) In Figure S5G of the originally published version of this article, the authors mistakenly included H&E sections from the pancreas rather than liver. Additionally, “NuPAGE” was incorrectly written as “Nu-AGE” in the key resources table under the subheading “Chemicals, peptides, and recombinant proteins.” The authors also mistakenly wrote “amantadine” instead of “anandamide” in the sentence that now reads “The endocannabinoid anandamide is made on-demand, unlike classical neurotransmitters (Di Marzo et al., 1994), and causes vasodilation, bradycardia, and hypotension (Movahed et al., 2005).” Figure S5G has now been replaced with the correct image, and all other errors have been corrected online. The authors apologize for any confusion that they may have caused.Figure S5Assessment of the effects of genistein on D9 -THC-induced effects in C57BL/6J mouse model, related to Figure 6 (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT) Cannabinoid receptor 1 antagonist genistein attenuates marijuana-induced vascular inflammationWei et al.CellApril 29, 2022In BriefMarijuana use is on the rise and is associated with cardiovascular disease. Δ9-tetrahydrocannabinol (Δ9-THC), the psychedelic component of marijuana, causes vascular inflammation, oxidative stress, and atherosclerosis via cannabinoid receptor 1. Genistein, a soybean isoflavone, blocks harmful cardiovascular effects of Δ9-THC while preserving clinically useful effects such as sedation and analgesia. Full-Text PDF Open Archive