摘要
在过去的几十年里,预期寿命的延长和富含饱和脂肪和糖的食物的消费增加了普通人群的健康问题。 代谢综合征(MS)是一组由肥胖、血脂异常、高血糖和高血压等因素组成的疾病,在工业化国家和发展中国家迅速增加。导致性早熟与年龄相关的疾病。事实上,氧化应激、晚期糖基化终末产物的积聚,以及慢性低度炎症是MS和理疗的共同特征。合乎逻辑的老化。特别是,所有的MS因子都促进了一种叫做Metaflamation的炎症状态的发展,这种炎症状态与早期先天imm的激活有关。通过多蛋白复合物炎症体的组装反应。炎症分子平台的研究最多的是含有(Nlrp)3的类结节样受体吡啶。在多种外源和内源性刺激作用下,caspase-1和IL-1β依次被切割,随后分泌活性IL-1β。我们在这里收集关于NLRP 3的最新发现。MS的激活,为其在代谢的靶组织中的疾病进展和器官功能障碍提供了证据,特别是在心血管、肝和肾并发症中。NS,专注于氧化应激和晚期糖基化终末产物。关于调节NLRP 3激活和相关代谢影响的最有希望的策略的一个广泛的概述是也提供了,因为找到特定的药理学工具是一项迫切的要求,以减轻社会和经济负担的MS-和老年相关疾病。
关键词: 代谢综合征,二甲双胍,NLRP 3炎症,氧化应激,衰老,心肌缺血/再灌注,脂肪性肝炎,慢性肾病。
Current Medicinal Chemistry
Title:Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome
Volume: 25 Issue: 11
关键词: 代谢综合征,二甲双胍,NLRP 3炎症,氧化应激,衰老,心肌缺血/再灌注,脂肪性肝炎,慢性肾病。
摘要: In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems.
The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.
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Cite this article as:
Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome, Current Medicinal Chemistry 2018; 25 (11) . https://dx.doi.org/10.2174/0929867324666170407123522
DOI https://dx.doi.org/10.2174/0929867324666170407123522 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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