Potential mechanisms linking atherosclerosis and increased cardiovascular risk in COPD: focus on Sirtuins.

Potential mechanisms linking atherosclerosis and increased cardiovascular risk in COPD: focus on Sirtuins.
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DOI:
10.3390/ijms140612696
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发表时间:
2013-06-17
影响因子:
5.6
通讯作者:
Ferrara N
Ferrara N
中科院分区:
生物学2区
文献类型:
--
作者:
Corbi G;Bianco A;Turchiarelli V;Cellurale M;Fatica F;Daniele A;Mazzarella G;Ferrara N

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动脉粥样硬化的发展是一个多步骤的过程,至少部分受血管内皮功能的控制。在人类和动脉粥样硬化实验模型中的观察已经确定单核细胞募集是动脉粥样硬化形成的早期事件。慢性炎症与衰老及其相关疾病(例如,动脉粥样硬化和慢性阻塞性肺病)。最近发现,Sirtuins(NAD+依赖性脱乙酰酶)是长寿和健康的关键调节因子。它们似乎在血管生物学中具有突出的作用,并调节年龄依赖性动脉粥样硬化的各个方面。许多研究表明SIRT 1在体外表现出抗炎特性(例如,脂肪酸诱导的炎症),体内(例如,动脉粥样硬化、基因敲除小鼠正常免疫功能的维持)和临床研究(例如,慢性阻塞性肺疾病患者)。由于暴露于香烟烟雾的啮齿动物肺和慢性阻塞性肺疾病(COPD)患者肺中的SIRT 1显著减少,SIRT 1的激活可能是慢性阻塞性肺疾病治疗的潜在靶点。我们综述了COPD-CVD共存的炎症机制以及SIRT 1在这些系统调节中的潜在作用。
The development of atherosclerosis is a multi-step process, at least in part controlled by the vascular endothelium function. Observations in humans and experimental models of atherosclerosis have identified monocyte recruitment as an early event in atherogenesis. Chronic inflammation is associated with ageing and its related diseases (e.g., atherosclerosis and chronic obstructive pulmonary disease). Recently it has been discovered that Sirtuins (NAD+-dependent deacetylases) represent a pivotal regulator of longevity and health. They appear to have a prominent role in vascular biology and regulate aspects of age-dependent atherosclerosis. Many studies demonstrate that SIRT1 exhibits anti-inflammatory properties in vitro (e.g., fatty acid-induced inflammation), in vivo (e.g., atherosclerosis, sustainment of normal immune function in knock-out mice) and in clinical studies (e.g., patients with chronic obstructive pulmonary disease). Because of a significant reduction of SIRT1 in rodent lungs exposed to cigarette smoke and in lungs of patients with chronic obstructive pulmonary disease (COPD), activation of SIRT1 may be a potential target for chronic obstructive pulmonary disease therapy. We review the inflammatory mechanisms involved in COPD-CVD coexistence and the potential role of SIRT1 in the regulation of these systems.
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