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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:7.)
© 2009 American Heart Association, Inc.

Editorials

Cannabinoid CB₁ Receptor Antagonists for Atherosclerosis and Cardiometabolic Disorders

New Hopes, Old Concerns?

Pál Pacher

From the Sections on Oxidative Stress Tissue Injury, Laboratory of Physiological Studies, NIAAA, National Institutes of Health, Bethesda, Md.

Correspondence to Pál Pacher, MD, PhD, FAPS, FAHA, Section on Oxidative Stress Tissue Injury, Laboratory of Physiologic Studies/NIAAA, National Institutes of Health, 5625 Fishers Lane, MSC-9413, Bethesda, MD 20892-9413. E-mail pacher@mail.nih.gov

Key Words: cardiovascular • endocannabinoids • atherosclerosis • myocardial infarction • metabolic syndrome • diabetes

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The endocannabinoid system (EC) system is a recently characterized physiological system that comprises the G protein–coupled CB₁ and CB₂, as well as additional yet unidentified receptors, their endogenous ligands termed endocannabinoids (lipid mediators generated in the brain and peripheral tissues, which elicit a broad range of biological effects similar to those of marijuana), and the enzymes and membrane transporter(s) involved in the biosynthesis/degradation and cellular uptake/release of these lipid mediators.¹ The dysregulation of the endocannabinoid system has recently been implicated in numerous human diseases, and its pharmacological modulation is a very promising strategy to treat various inflammatory, neurodegenerative, cardiovascular, metabolic disorders, ischemia/reperfusion damage, as well as cancer and pain.^1,2 CB₂ receptors are predominantly expressed in immune and hematopoietic cells, but to a lesser extent also in the myocardium, and in coronary endothelial and smooth muscle cells.^1,3 Activation of CB₂ receptors mediates various antiinflammatory and immunosuppressive effects,¹ and has recently been shown to attenuate atherosclerosis progression in an apolipoprotein E knockout mouse model of the disease, presumably by reducing the proliferative capacity and interferon (INF)- production of lymphoid cells, and inhibiting macrophage chemotaxis and migration.⁴ CB₂ receptors activation also attenuates the tumor necrosis factor (TNF)-– or bacterial endotoxin (lipopolysaccharide [LPS])-induced vascular inflammatory response, and inflammation associated with ischemic reperfusion injury.^3,5 The CB₁ receptor is widely distributed in the central nervous system and at lower levels in various peripheral tissues (eg, myocardium, adipose tissue, liver, etc), and it has been shown to play an important role in regulating body weight, . . . [Full Text of this Article]

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