摘要
动脉粥样硬化及其主要的急性并发症心肌梗死和中风,是在世界范围内的导致死亡和发病率的主要原因。尽管心血管干预和医疗保健的重大进展,改善预防保健和治疗仍然是心血管研究一个持续的使命。在过去的10到15年,内源性大麻素系统已成为一个重要的脂质信号系统参与许多生物学过程。越来越多的证据表明,内源性大麻素CB1受体信号通路的过度表达促进了如肥胖、胰岛素抵抗及血脂异常等心血管危险因素的发展。这促使研究内源性大麻素系统在动脉粥样硬化中的作用越来越大的兴趣。相对于CB1信号不利的行动,内源性大麻素CB2受体轴具有抗炎和抗动脉粥样硬化的作用。我们将回顾从实验和临床研究旨在了解内源性大麻素在心血管疾病信号中复杂的活动,这是一个新兴的目标,作为可能的治疗干预。
关键词: 大麻素受体CB1,CB2,甘油二酯脂肪酶,类花生酸,脂肪酸酰胺水解酶,单酰基甘油脂肪酶。
图形摘要
Current Drug Targets
Title:The Activated Endocannabinoid System in Atherosclerosis: Driving Force or Protective Mechanism?
Volume: 16 Issue: 4
Author(s): Sabine Steffens and Pal Pacher
Affiliation:
关键词: 大麻素受体CB1,CB2,甘油二酯脂肪酶,类花生酸,脂肪酸酰胺水解酶,单酰基甘油脂肪酶。
摘要: Atherosclerosis and its major acute complications, myocardial infarction and stroke, are the leading causes of death and morbidity worldwide. Despite major advances in cardiovascular intervention and healthcare, improving preventive care and treatment remains a continuous mission for cardiovascular research. Within the last 10 to 15 years, the endocannabinoid system has emerged as an important lipid signaling system involved in many biological processes. Growing evidence suggests that an overactive endocannabinoid-CB1 receptor signaling promotes the development of cardiovascular risk factors such as obesity, insulin resistance and dyslipidemia. This prompted an increasing interest in studying the role of the endocannabinoid system in atherosclerosis. As opposed to the detrimental actions of CB1 signaling, the endocannabinoid-CB2 receptor axis exhibits an anti-inflammatory and atheroprotective role. We will review recent findings from experimental and clinical studies aimed at understanding the complex actions of endocannabinoid signaling in cardiovascular disease. This is followed by an outlook on emerging targets for possible therapeutic intervention.
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Cite this article as:
Sabine Steffens and Pal Pacher , The Activated Endocannabinoid System in Atherosclerosis: Driving Force or Protective Mechanism?, Current Drug Targets 2015; 16 (4) . https://dx.doi.org/10.2174/1389450115666141202113225
DOI https://dx.doi.org/10.2174/1389450115666141202113225 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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