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首页> 外文期刊>Biochemistry >Molecular mechanisms of latent inflammation in metabolic syndrome. Possible role of sirtuins and peroxisome proliferator-activated receptor type gamma
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Molecular mechanisms of latent inflammation in metabolic syndrome. Possible role of sirtuins and peroxisome proliferator-activated receptor type gamma

机译:代谢综合征中潜在炎症的分子机制。 sirtuins和过氧化物酶体增殖物激活受体类型γ的可能作用

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摘要

The problem of metabolic syndrome is one of the most important in medicine today. The main hazard of metabolic syndrome is development of latent inflammation in adipose tissue, which promotes atherosclerosis, non-alcoholic fatty liver disease, myocarditis, and a number of other illnesses. Therefore, understanding of molecular mechanisms of latent inflammation in adipose tissue is very important for treatment of metabolic syndrome. Three main components that arise during hypertrophy and hyperplasia of adipocytes underlie such inflammation: endoplasmic reticulum stress, oxidative stress, and hypoxia. Each of these components mediates activation in different ways of the key factor of inflammation-NF-kappa B. For metabolic syndrome therapy, it is suggested to influence a number of inflammatory signaling components by activating other cell factors to suppress development of inflammation. Such potential factors are peroxisome proliferator-activated receptors type gamma that suppress transcription factor NF-kappa B through direct contact or via kinase of a NF-kappa B inhibitor (IKK), and also the antiinflammatory transcription factor AP-1. Other possible targets are type 3 NAD(+)-dependent histone deacetylases (sirtuins). There are mutually antagonistic relationships between NF-kappa B and sirtuin type 1 that prevent development of inflammation in metabolic syndrome. Moreover, sirtuin type 1 inhibits the antiinflammatory transcription factor AP-1. Study of the influence of these factors on the relationship between macrophages and adipocytes, macrophages, and adipose tissue-derived stromal cells can help to understand mechanisms of signaling and development of latent inflammation in metabolic syndrome.
机译:代谢综合征的问题是当今医学中最重要的问题之一。代谢综合症的主要危害是脂肪组织中潜在性炎症的发展,这会促进动脉粥样硬化,非酒精性脂肪肝,心肌炎和许多其他疾病。因此,了解脂肪组织中潜在炎症的分子机制对于代谢综合征的治疗非常重要。在脂肪细胞肥大和增生过程中出现的三个主要成分是这种炎症的基础:内质网应激,氧化应激和缺氧。这些成分中的每一个都以不同的方式介导炎症关键因子NF-κB的激活。对于代谢综合征治疗,建议通过激活其他细胞因子来抑制炎症发展,从而影响许多炎症信号传导成分。此类潜在因素是过氧化物酶体增殖物激活的γ型受体,可通过直接接触或通过NF-κB抑制剂(IKK)的激酶抑制转录因子NF-κB,以及抗炎转录因子AP-1。其他可能的目标是3型NAD(+)依赖性组蛋白脱乙酰基酶(sirtuins)。 NF-κB和sirtuin 1型之间存在相互拮抗的关系,可防止代谢综合征中炎症的发展。此外,Sirtuin 1型抑制抗炎转录因子AP-1。研究这些因素对巨噬细胞与脂肪细胞,巨噬细胞和脂肪组织来源的基质细胞之间关系的影响,有助于理解代谢综合征潜伏性炎症的信号传导和发展机制。

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