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Verfasst von:Guillamat-Prats, Raquel [VerfasserIn]   i
 Herzig, Stephan [VerfasserIn]   i
Titel:Endocannabinoid signalling in atherosclerosis and related metabolic complications
Verf.angabe:Raquel Guillamat-Prats, Martina Rami, Stephan Herzig, Sabine Steffens
E-Jahr:2019
Jahr:15. Februar 2019
Umfang:9 S.
Fussnoten:Gesehen am 29.01.2020
Titel Quelle:Enthalten in: Thrombosis and haemostasis
Ort Quelle:Stuttgart : Thieme, 1976
Jahr Quelle:2019
Band/Heft Quelle:119(2019), 4, Seite 567-575
ISSN Quelle:2567-689X
Abstract:Endocannabinoids are a group of arachidonic acid-derived lipid mediators binding to cannabinoid receptors CB1 and CB2. An overactivity of the endocannabinoid system plays a pathophysiological role in the development of visceral obesity and insulin resistance. Moreover, elevated circulating endocannabinoid levels are also prevalent in atherosclerosis. The pathophysiological increase of endocannabinoid levels is due to an altered expression of endocannabinoid synthesizing and degrading enzymes induced by inflammatory mediators such as cytokines or lipids. Emerging experimental evidence suggests that enhanced endocannabinoid signalling affects atherosclerosis via multiple effects, including a modulation of vascular inflammation, leukocyte recruitment, macrophage cholesterol metabolism and consequently atherosclerotic plaque stability. In addition, recent findings in various metabolic disease models highlight the relevance of peripheral CB1 cannabinoid receptors in adipose tissue, liver and pancreas, which crucially regulate lipid and glucose metabolism as well as macrophage properties in these organs. This suggests that targeting the endocannabinoid system in the vasculature and peripheral organs might have a therapeutic potential for atherosclerosis by inhibiting vascular inflammation and improving metabolic risk factors. This review will provide a brief update on the effects of endocannabinoid signalling in atherosclerosis and related metabolic complications.
DOI:doi:10.1055/s-0039-1678738
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1055/s-0039-1678738
 Verlag: http://www.thieme-connect.de/DOI/DOI?10.1055/s-0039-1678738
 DOI: https://doi.org/10.1055/s-0039-1678738
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1688791574
Verknüpfungen:→ Zeitschrift

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