The role of the endocannabinoid system in atherosclerosis
Autor: | François Mach, Sabine Steffens |
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Rok vydání: | 2008 |
Předmět: |
medicine.medical_specialty
Endocrinology Diabetes and Metabolism medicine.medical_treatment Inflammation/etiology Receptor Cannabinoid CB2/physiology Inflammation Cardiovascular System Models Biological Pathogenesis Receptor Cannabinoid CB2 Cellular and Molecular Neuroscience Endocrinology Immune system Receptor Cannabinoid CB1 Atherosclerosis/complications/etiology Internal medicine Cannabinoid Receptor Modulators Medicine Cardiovascular System/drug effects Animals Humans Platelet activation Receptor ddc:616 Metabolic Syndrome Endocrine and Autonomic Systems business.industry Cannabinoids medicine.disease Atherosclerosis Endocannabinoid system Neurosecretory Systems/physiology Neurosecretory Systems Endocannabinoids/physiology Cannabinoids/pharmacology Receptor Cannabinoid CB1/antagonists & inhibitors Cannabinoid Metabolic syndrome medicine.symptom Metabolic Syndrome X/complications business Endocannabinoids |
Zdroj: | Journal of neuroendocrinology, Vol. 20 Suppl 1 (2008) pp. 53-7 |
ISSN: | 1365-2826 |
Popis: | Our current understanding of the pathophysiology of atherosclerosis suggests a prominent role for immune responses from its initiation through its complications. Given the increasing prevalence of cardiovascular risk factors worldwide, there is an urgent need to better understand the underlying mechanisms to improve current treatment protocols. A growing body of evidence suggests that endocannabinoid signalling plays a critical role in the pathogenesis of atherogenesis and its clinical manifestations. Blocking CB(1) receptors has been shown to mediate not only weight reduction, but also several cardiometabolic effects in rodents and humans, indicating a potential relevance for the process of atherosclerosis. Activation of CB(2) receptors with Delta(9)-tetrahydrocannabinol (THC) has been shown to inhibit atherosclerotic plaque progression in mice, mainly by inhibiting macrophage recruitment. Endocannabinoids released from endothelial cells, macrophages or platelets, reduce hypertension in rodents, a major risk factor for atherosclerosis. In addition, anandamide inhibits inflammatory gene expression in endothelial cells, and consequently monocyte adhesion. Conversely, endocannabinoids might also mediate pro-atherosclerotic effects by inducing platelet activation. In conclusion, the precise role of the endocannabinoid system during atherosclerosis is not yet understood. Whether increased endocannabinoid signalling is associated with disease progression and increased risk of acute thrombotic events remains to be determined. |
Databáze: | OpenAIRE |
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