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脓毒症发病机制中的分子机制。

Molecular mechanisms in the pathogenesis of sepsis.

作者信息

Pop-Began V, Păunescu V, Grigorean V, Pop-Began D, Popescu C

机构信息

"Carol Davila" University of Medicine and Pharmacy, Bucharest; Department of General Surgery, "Bagdasar - Arseni" Clinical Emergency Hospital, Bucharest.

Department of Public Health and Health Management, "Carol Davila" University of Medicine and Pharmacy, Bucharest.

出版信息

J Med Life. 2014;7 Spec No. 2(Spec Iss 2):38-41.

PMID:25870671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4391358/
Abstract

Innate immune system is a universal form of host defense against infections. The recognition of the innate immunity is based on a limited number of encoded receptors that have evolved to recognize microbial metabolism products. The recognition of these molecular structures allows the immune system to distinguish its own infectious components from non-communicable structures. The immune suppression is a hallmark of sepsis. The complement system is activated in the early stages of sepsis, generating large amounts of anaphylatoxin C5a. Complement and TLRs (toll-like receptors) family are two major upstream sensors and effectors systems of innate immunity. It was found that TLR4 and complement system are involved in the initiation of the inflammatory response in sepsis. Clinical studies in which TLR4 was blocked have not shown beneficial effects. TLRs, that are a subfamily of PRRs (pattern recognition receptors), have emerged as the crucial receptors for the recognition of DAMPs (Damage-associated molecular pattern molecules). Recently, a special form of non-coding genetic material called microRNA has been highlighted in the complex cascade of sepsis. The individual role of every microRNA and the exact role of microRNA network are under investigation. Currently, studies are performed in order to find micro RNA to be used as biomarkers of sepsis. Researches are performed to determine microRNA, small fragments of non-coding RNA, in order to distinguish between patients with sepsis and healthy patients, and if the plasma levels of microRNA correlate with the severity of the disease. Recent researches report that the regulation of gene expression through microRNA plays a very important role in the following cellular processes, for example: apoptosis, the differentiation process, and the cell cycle.

摘要

先天性免疫系统是宿主抵御感染的一种普遍形式。对先天性免疫的识别基于有限数量的编码受体,这些受体经过进化以识别微生物代谢产物。对这些分子结构的识别使免疫系统能够区分自身的感染成分和非感染性结构。免疫抑制是脓毒症的一个标志。补体系统在脓毒症早期被激活,产生大量过敏毒素C5a。补体和Toll样受体(TLRs)家族是先天性免疫的两个主要上游传感器和效应系统。研究发现,TLR4和补体系统参与了脓毒症炎症反应的启动。阻断TLR4的临床研究并未显示出有益效果。TLRs是模式识别受体(PRRs)的一个亚家族,已成为识别损伤相关分子模式分子(DAMPs)的关键受体。最近,一种名为微小RNA的特殊形式的非编码遗传物质在脓毒症的复杂级联反应中受到关注。每个微小RNA的个体作用以及微小RNA网络的确切作用正在研究中。目前,正在进行研究以寻找可作为脓毒症生物标志物的微小RNA。研究旨在确定微小RNA(非编码RNA的小片段),以区分脓毒症患者和健康患者,以及微小RNA的血浆水平是否与疾病严重程度相关。最近的研究报告称,通过微小RNA对基因表达的调控在以下细胞过程中起着非常重要的作用,例如:细胞凋亡、分化过程和细胞周期。

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本文引用的文献

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Identification of microRNA as sepsis biomarker based on miRNAs regulatory network analysis.基于微小RNA调控网络分析鉴定微小RNA作为脓毒症生物标志物
Biomed Res Int. 2014;2014:594350. doi: 10.1155/2014/594350. Epub 2014 Apr 6.
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Post challenge inhibition of C3 and CD14 attenuates Escherichia coli-induced inflammation in human whole blood.补体 C3 和 CD14 抑制后可减轻人全血中大肠杆菌诱导的炎症反应。
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Integrative network analysis reveals active microRNAs and their functions in gastric cancer.
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在脂多糖诱导的脓毒症小鼠模型中表现出抗炎活性。
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A system pharmacology Boolean network model for the TLR4-mediated inflammatory response in early sepsis.TLR4 介导的早期脓毒症炎症反应的系统药理学布尔网络模型。
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The Landscape of Featured Metabolism-Related Genes and Imbalanced Immune Cell Subsets in Sepsis.脓毒症中特征性代谢相关基因及免疫细胞亚群失衡的概况
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DNA-Aptamer Raised against Receptor for Advanced Glycation End Products Improves Survival Rate in Septic Mice.针对晚期糖基化终产物受体的 DNA-适体可提高脓毒症小鼠的生存率。
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Parallels in Sepsis and COVID-19 Conditions: Implications for Managing Severe COVID-19.脓毒症和 COVID-19 病症的相似之处:对重症 COVID-19 管理的启示。
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Revisited-Crosstalk between microRNA Expression, Inflammation, Oxidative Stress, and Endocannabinoid Response System in Critically Ill Patients with Sepsis.危重病脓毒症患者中 microRNA 表达、炎症、氧化应激和内源性大麻素反应系统的串扰。
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