Journal Article

DZNE-2026-00718

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Endothelial cannabinoid CB1 receptor deficiency reduces shear stress-induced arterial inflammation and lipid uptake.

Chen, B. ; Prabhu, A. ; Li, G. ; Kaltenbach, A. ; Wang, Y. ; Shakir, G. ; Natarelli, L. ; Megens, R. ; Jansen, Y. ; Ramanathan, S. ; Geiger, M. ; Faussner, A. ; Hristov, M. ; Richter, D. ; Di, X. ; van der Stelt, M. ; Triantafyllidou, V. ; Li, Z. ; Sachs, N. ; Paloschi, V. ; Maegdefessel, L. ; Hofmann, S. M. ; Schifferer, M.DZNE* ; Simons, M.DZNE* ; Weber, C. ; Santovito, D. ; Herzig, S. ; Guillamat Prats, R. ; Steffens, S.

2026
Springer Nature [London]

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Please use a persistent id in citations: doi:10.1038/s41467-026-75214-2

Abstract: Peripheral cannabinoid CB1 receptor antagonists that lack central nervous system effects are emerging as promising therapies for metabolic disease, yet the role of endothelial CB1 signaling in atherosclerosis remains unclear. Here, we show that endothelial CB1 is expressed in human atherosclerotic plaques, is induced by oscillatory shear stress in atheroprone flow regions, and promotes vascular inflammation, permeability and lipid uptake. Endothelial-specific Cnr1 deletion or peripheral CB1 antagonism in mice attenuates atherosclerosis, reduces endothelial caveolae-dependent low-density lipoprotein uptake by downregulating caveolin-1 and ALK1 expression, and improves metabolic parameters in brown and white adipose tissue and the liver. The anti-atherogenic and metabolic effects are more pronounced in females, which is possibly linked to estrogen signaling. These findings identify endothelial CB1 as a proatherogenic, sex-biased regulator of vascular lipid transport and plaque development and associated metabolic dysfunction.

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Contributing Institute(s):

1. Neuronal Cell Biology (AG Misgeld)
2. Clinical Research (Munich) (Clinical Research (Munich))

Research Program(s):

1. 351 - Brain Function (POF4-351) (POF4-351)
2. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

Appears in the scientific report 2026

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