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摘要
哺乳动物的sirtuins(SIRT-7)是依赖NAD+去乙酰化酶在时效以及大范围细胞功能起到重要的角色。SIRT1,该家族最具有特色的成员,作为一个传感器的氧化还原状态,并触发细胞中适当的防御反应。大部分针具显示SIRT1通过阻止由压力引起的凋亡和衰老诱导心血管系统中细胞和系统性保护作用,减缓内皮机能失调。因此,SIRT1可作为大部分心血管疾病具有潜力的治疗靶点。近期表明激活SIRT1也可认为是保护神经的一种措施。而且,SIRT1在体内外都能保护防止缺血或再灌注的发生,通过保留脑血流量来避免严重的缺血性损伤。在过去的几年里有证明显示其他的sirtuins特别是SIRT3和SIRT6能够对心血管症状产生有益的作用。本文的目的是为了描述和讨论近期关于SIRT1和其他sirtuins在心血管的试验证明心脑血管疾病影响的试验证据,强调了这些酶在这些情况下的治疗和预防潜在的治疗性效应。
关键词: SIRT1
Current Drug Targets
Title:Sirtuins: Possible Clinical Implications in Cardio and Cerebrovascular Diseases
Volume: 18 Issue: 4
关键词: SIRT1
摘要: Mammalian sirtuins (SIRT1-7) are NAD+-dependent deacetylases, which play an important role in aging and in a wide range of cellular functions. SIRT1, the best-characterized member of the family, acts as a sensor of the redox state and triggers in the cell the appropriate defense response. A large body of evidence has showed that SIRT1 induces both cellular and systemic protective effects in the cardiovascular system by preventing stress-induced apoptosis and senescence, and mitigating endothelial dysfunction. Hence, SIRT1 is now foreseen as a potential therapeutic target for a growing number of cardiovascular diseases. Recently, it has been suggested that SIRT1 activation could also be considered as a neuroprotective strategy. Indeed, SIRT1 protects against ischemia/reperfusion injury both in vitro and in vivo and avoids severe ischemic damage by preserving cerebral blood flow. In the last years it was suggested that others sirtuins, in particular SIRT3 and SIRT6, could exert beneficial effects in vascular syndromes. The aim of this review was to describe and discuss recent experimental evidence on the effects of SIRT1 and other sirtuins on the pathophysiology of cardio- and cerebrovascular diseases, underlying a potential therapeutic effect of these enzymes in the treatment and/or prevention of such conditions.
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Sirtuins: Possible Clinical Implications in Cardio and Cerebrovascular Diseases, Current Drug Targets 2017; 18 (4) . https://dx.doi.org/10.2174/1389450116666151019095903
DOI https://dx.doi.org/10.2174/1389450116666151019095903 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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