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Pathway-Based Analysis of the Liver Response to Intravenous Methylprednisolone Administration in Rats: Acute Versus Chronic Dosing. 基于途径的大鼠静脉注射甲基强的松龙肝脏反应分析:急性与慢性给药。
Pub Date : 2019-04-15 eCollection Date: 2019-01-01 DOI: 10.1177/1177625019840282
Alison Acevedo, Ana Berthel, Debra DuBois, Richard R Almon, William J Jusko, Ioannis P Androulakis

Pharmacological time-series data, from comparative dosing studies, are critical to characterizing drug effects. Reconciling the data from multiple studies is inevitably difficult; multiple in vivo high-throughput -omics studies are necessary to capture the global and temporal effects of the drug, but these experiments, though analogous, differ in (microarray or other) platforms, time-scales, and dosing regimens and thus cannot be directly combined or compared. This investigation addresses this reconciliation issue with a meta-analysis technique aimed at assessing the intrinsic activity at the pathway level. The purpose of this is to characterize the dosing effects of methylprednisolone (MPL), a widely used anti-inflammatory and immunosuppressive corticosteroid (CS), within the liver. A multivariate decomposition approach is applied to analyze acute and chronic MPL dosing in male adrenalectomized rats and characterize the dosing-dependent differences in the dynamic response of MPL-responsive signaling and metabolic pathways. We demonstrate how to deconstruct signaling and metabolic pathways into their constituent pathway activities, activities which are scored for intrinsic pathway activity. Dosing-induced changes in the dynamics of pathway activities are compared using a model-based assessment of pathway dynamics, extending the principles of pharmacokinetics/pharmacodynamics (PKPD) to describe pathway activities. The model-based approach enabled us to hypothesize on the likely emergence (or disappearance) of indirect dosing-dependent regulatory interactions, pointing to likely mechanistic implications of dosing of MPL transcriptional regulation. Both acute and chronic MPL administration induced a strong core of activity within pathway families including the following: lipid metabolism, amino acid metabolism, carbohydrate metabolism, metabolism of cofactors and vitamins, regulation of essential organelles, and xenobiotic metabolism pathway families. Pathway activities alter between acute and chronic dosing, indicating that MPL response is dosing dependent. Furthermore, because multiple pathway activities are dominant within a single pathway, we observe that pathways cannot be defined by a single response. Instead, pathways are defined by multiple, complex, and temporally related activities corresponding to different subgroups of genes within each pathway.

药理学时间序列数据(来自给药对比研究)对于描述药物效应至关重要。要想捕捉药物的全局和时间效应,必须进行多项体内高通量组学研究,但这些实验虽然类似,但在(微阵列或其他)平台、时间尺度和给药方案上各不相同,因此无法直接合并或比较。本研究采用荟萃分析技术解决了这一协调问题,该技术旨在评估通路层面的内在活性。其目的是描述甲基强的松龙(MPL)(一种广泛使用的抗炎和免疫抑制皮质类固醇(CS))在肝脏内的剂量效应。我们采用多元分解法分析了雄性肾上腺切除大鼠的急性和慢性 MPL 剂量,并描述了 MPL 信号传导和代谢通路的动态响应随剂量变化而产生的差异。我们展示了如何将信号传导和代谢通路解构为其组成通路活动,并对这些活动的内在通路活动进行评分。我们采用基于模型的途径动态评估方法,将药代动力学/药效动力学(PKPD)原理延伸到途径活动的描述中,比较了剂量引起的途径活动动态变化。这种基于模型的方法使我们能够假设可能出现(或消失)的间接剂量依赖性调控相互作用,从而指出剂量对 MPL 转录调控可能产生的机理影响。急性和慢性 MPL 给药都会诱导以下通路家族的核心活动:脂质代谢、氨基酸代谢、碳水化合物代谢、辅因子和维生素代谢、重要细胞器的调节以及异生物代谢通路家族。在急性和慢性用药期间,途径活动会发生变化,这表明 MPL 的反应与用药量有关。此外,由于单个通路中多种通路活动占主导地位,我们发现通路不能由单一反应来定义。相反,通路是由与每条通路中不同基因亚群相对应的多种复杂且与时间相关的活动来定义的。
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引用次数: 0
Temporal and Spatial Differential Expression of Glutamate Receptor Genes in the Brain of Down Syndrome 唐氏综合征脑组织谷氨酸受体基因的时空差异表达
Pub Date : 2019-03-13 DOI: 10.5772/INTECHOPEN.82446
A. Ortiz, Mailyn Alejandra Bedoya Saldarriaga, Julio César Montoya Villegas, F. García-Vallejo
Studying the dysregulation of expression of glutamate receptors is crucial to better understand the mechanisms associated with cognitive disabilities in Down syndrome (DS) patients. By using data of microarray experiments previously deposited in GEO Dataset, we studied the expression of 26 glutamate receptor genes in DS brain samples since prenatal to adult age in several brain structures. Overall, our results showed a complexity in the expression of the genes which were depen-dent mainly on the brain structure analyzed; especially, the hippocampus showed a different expression pattern. While in the general brain analysis the overexpressed genes were GRIN3A and GRIN2C, higher expression levels of GRM1, GRID2, and GRIK1 gene receptors were recorded in hippocampus. Our results suggest that the glutamatergic system in association with other neurotransmitter systems in the human brain would associate with glutamatergic receptor alterations to bring upon synaptic changes and cognitive deficits in DS models.
研究谷氨酸受体的表达失调对于更好地理解唐氏综合征(DS)患者认知障碍的相关机制至关重要。利用GEO数据集的微阵列实验数据,我们研究了26个谷氨酸受体基因在DS脑样本中从产前到成年的几种脑结构中的表达。总的来说,我们的结果显示了基因表达的复杂性,这些基因主要取决于所分析的大脑结构;特别是海马体表现出不同的表达模式。在一般的大脑分析中,过表达的基因是GRIN3A和GRIN2C,而在海马中,GRM1、GRID2和GRIK1基因受体的表达水平较高。我们的研究结果表明,人类大脑中与其他神经递质系统相关的谷氨酸能系统可能与谷氨酸能受体的改变相关,从而导致DS模型的突触改变和认知缺陷。
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引用次数: 0
Introductory Chapter: Gene Regulation, an RNA Network-Dependent Architecture 导论章:基因调控,RNA网络依赖的结构
Pub Date : 2019-02-11 DOI: 10.5772/INTECHOPEN.84535
P. Behzadi, Lernik Issakhanian
Genetics is known as an old and ancient science that its origination goes back to at least 7000 years ago. Iranians are one of the earliest pioneers in genetics from ancient world. The brilliant Iranian (Persian) literature epic of Shahnameh edited by the Iranian shining star literate “Abolqasem Ferdowsi Toosi” is an invaluable evidence to prove this claim. By the time and progression in biology, the superamazing molecule of DNA was discovered. Today, we know that the unique molecule of DNA involves the genetic and vital data within its bases as constitutional structures of nucleotides. Both eukaryotic and prokaryotic chromosomes are made up of DNA molecules. In addition to DNAs, the role and importance of RNAs are not lesser than DNAs [1]. In 1953, the interesting structure of DNA molecule with anti-parallel doublehelix architecture was recognized by Watson and Crick. In 1958, the hypothesis of central dogma of molecular biology was published by Crick in which he described the translation of genetic language located on DNA into amino acid sequences of protein by the transient molecule of RNA (mainly messenger RNA (mRNA)). The primitive biological characteristics of mRNA were recognized in 1961, while these properties regarding ribosomal RNA (rRNA) and transfer RNA (tRNA) molecules were determined in the 1950s [2].
遗传学被认为是一门古老的科学,它的起源至少可以追溯到7000年前。伊朗人是古代世界最早的遗传学先驱之一。由伊朗明星文学家“Abolqasem Ferdowsi Toosi”编辑的辉煌的伊朗(波斯)文学史诗Shahnameh是证明这一说法的宝贵证据。随着时间的推移和生物学的进步,超级神奇的DNA分子被发现了。今天,我们知道独特的DNA分子包含了核苷酸构成结构的遗传和重要数据。真核生物和原核生物的染色体都由DNA分子组成。除dna外,rna的作用和重要性也不低于dna[1]。1953年,沃森和克里克发现了DNA分子具有反平行双螺旋结构的有趣结构。1958年,克里克(Crick)发表了分子生物学中心法则假说,描述了瞬时分子RNA(主要是信使RNA (mRNA))将位于DNA上的遗传语言翻译成蛋白质的氨基酸序列。mRNA的原始生物学特性在1961年被确认,而核糖体RNA (rRNA)和转移RNA (tRNA)分子的这些特性在20世纪50年代才被确定[2]。
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引用次数: 2
Model-based Evaluation of Gene Expression Changes in Response to Leishmania Infection. 利什曼原虫感染后基因表达变化的模型评价。
Pub Date : 2019-02-06 eCollection Date: 2019-01-01 DOI: 10.1177/1177625019828350
Brendan D Stamper, Madison Davis, Sean Scott-Collins, Julie Tran, Caryn Ton, Agapi Simidyan, Sigrid C Roberts

Since the development of high-density microarray technology in the late 1990s, global host gene expression changes in response to various stimuli have been extensively studied. More than a dozen peer-reviewed publications have investigated the effect of Leishmania infection in various models since 2001. This review covers the transcriptional changes in macrophage models induced by various Leishmania species and summarizes the resulting impact these studies have on our understanding of the host response to leishmaniasis in vitro. Characterization of the similarities and differences between various model systems will not only further our understanding of Leishmania-induced changes to macrophage gene expression but also identify potential therapeutic targets in the future.

自20世纪90年代末高密度微阵列技术发展以来,全球宿主基因表达在各种刺激下的变化得到了广泛的研究。自2001年以来,十几份同行评审的出版物调查了各种模型中利什曼原虫感染的影响。本文综述了各种利什曼原虫诱导的巨噬细胞模型的转录变化,并总结了这些研究对我们了解宿主对利什曼原虫体外反应的影响。表征各种模型系统之间的异同不仅将进一步加深我们对利什曼原虫诱导巨噬细胞基因表达变化的理解,而且还将确定未来潜在的治疗靶点。
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引用次数: 4
Gene Activation by the Cytokine-Driven Transcription Factor STAT1 细胞因子驱动转录因子STAT1的基因激活
Pub Date : 2019-01-24 DOI: 10.5772/INTECHOPEN.82699
R. Nast, Julia Staab, T. Meyer
Signal transducers and activators of transcription (STATs) are a family of cytokine-regulated transcription factors, which serve the dual role of external signal transduction and transcriptional activation. The founding member of this family, STAT1, is involved in a plethora of cellular processes, including interferon-dependent upregulation of various effector mechanisms in immune and non-immune cells to control bacterial, fungal and parasitic infections. In this chapter, we discuss the principles of STAT1-driven gene expression and focus on the clinical phenotypes of various human STAT1 mutations. In particular, we highlight the significance of sequence-specific DNA binding and intact nucleocytoplasmic shuttling for full transcriptional activation of interferon-driven target genes.
信号转导和转录激活因子(Signal transducers and activators of transcription, STATs)是一类细胞因子调控的转录因子,具有外部信号转导和转录激活的双重作用。这个家族的创始成员STAT1参与了大量的细胞过程,包括免疫和非免疫细胞中各种效应机制的干扰素依赖性上调,以控制细菌、真菌和寄生虫感染。在本章中,我们讨论了STAT1驱动基因表达的原理,并重点讨论了各种人类STAT1突变的临床表型。特别是,我们强调序列特异性DNA结合和完整的核细胞质穿梭对于干扰素驱动靶基因的完全转录激活的重要性。
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引用次数: 4
Reviewer List 审核人名单
Pub Date : 2019-01-01 DOI: 10.1177/2516865719829635
A. Elsalam, A. Adams, Murray Agirbasli, M. Akar, Nejat Akin, Muharram Akın, Melike Aksu, Emrullah Kokalj, N. Kostić, Jelena Kovač, Mirjana Kubisz, Peter Kukula, Krzysztof Kulkarni, Bipin Kulkarni, Roshni Kurtoglu, M. Lackner
List of Reviewer present in this pdf.
Abd Elsalam、Ahmed Adams、Murray Agirbasli、Mehmet Akar、Nejat Akin、Muharram Akın、Melike Aksu、Salih Alkhiary、Wael Alkim、Huseyin Ames、Paul Andó、Giuseppe Andrawes、Nevine Andreoli、Laura Arcelus、Juan Arnold、Donald Atas、Halil Atike、Tekeli Kunt Avram、Simona Awasthi、Namrata Ayada、Ceylan Bacher、Peter Bakcoul、Tamam Baker、Peter Bansal、Vinod Barco、Stefano Bautista、Maria Berkman,Samuel Bern、Murray Beyan、Cengiz Bingol、Zuleyha Bista、Durga Bittar、Luis Blostein、Mark Bosco、Paes Bosevski、Marijan Brown、Ashley Brunetti、Natale Daniele Buchtele、Nina Cacciapuoti、Federico Cakmakli、Hasan Campo、Gianluca Camporese、Giuseppe Canda、M.Tunc Canpolat、Ugur Cao、Wenjing Capparelli、Federio Caprini、Joseph Carter、Charles Casais、Patricia Castro、Vagner Celik、Turgay Cheen,陈文华、Chien An Chi、Lianli Christopher、Amy Chudej、Juraj Ciftci Arslan、Fatma Coccheri、Sergio Coen Herak、Desiree Coen、Matteo Cortina De La Rosa、Evelyn Cosmi、Erich Dalar、Levent Dan、Andrei De Grooth、Hj De La Morena Barrio、Marı́a Eugenia De Marco、Luigi De Stefano、Valerio Demir、Ahmet Muzaffer Demir、Muzaffeer Di Micco、Pierpaolo Dimakakos、Evangelos Divani,Afshin Diz Kucukkaya、Reyhan Fabris、Fabrizio Faioni、Elena Fanikos、John Faraoni、David Fareed、Jawed Favaloro、Emmanuel Fisher、William Gaini、Shahin Gandara、Esteban Gasparyan、Armen Yuri Ghosh、Kanjaksha Girolami、Antonio Gouin、Isabelle Govaert、Paul Graf、Maria Gris、Jean-Christophe Guler、Nil Gurel、Emre Haas、Sylvia Haas、Thorsten Harenberg、Job Hasimi、Adnan Hatou、Takaaki He,华·亨斯肯斯、伊冯娜·霍普彭斯特德、黛布拉·休斯顿、唐纳德·伊巴、Toshiaki Imberti、Davide Ince、Birsen Iqbal、Omer Isik Balci、Yasemin Issa、Maria Ito、Takashi Jeske、Walter Jezovnik、Mateja Jin、Guodong Kakuros、Nikolaos Kalodiki、Evi Kamal、Haris Kang、Rima Kapan、Murat Karabay、Can Karakurt、Sait Katsuya、Tomohiro Kavakli、Kaan Kawasugi、Kazuo Kaya、Hasan Kehrel、Beate Kell、Jonathan Keskin,Muhammed Kickler,Thomas《临床与应用血栓形成/止血》第25卷:1-2a作者2019文章重复使用指南:sagepub.com/journals-permissions DOI:10.1177/10760029619834177 journals.sagepub.com/home/cat
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引用次数: 0
Distinct E2F-Mediated Transcriptional Mechanisms in Cell Proliferation, Endoreplication and Apoptosis 不同e2f介导的细胞增殖、内复制和凋亡的转录机制
Pub Date : 2018-12-13 DOI: 10.5772/INTECHOPEN.82448
H. Komori, R. Iwanaga, A. Bradford, Keigo Araki, K. Ohtani
E2F and DP family proteins are evolutionally conserved transcription factors among higher eukaryotes. E2F and DP proteins typically form a heterodimeric complex, which controls cell proliferation by regulating expression of growth-related genes. In addition, E2F family proteins have roles in various cellular events that require the expression of context-specific genes. E2F proteins use distinct mechanisms to regulate context-specific genes in different circumstances. The primary goal of this chapter is to compare three distinct mechanisms of mammalian E2F-mediated transcriptional regulation that control cell proliferation, endoreplication and apoptosis. Briefly, E2F7 and E2F8 control endoreplication by suppressing the expression of their target genes. They do not require DP or pRb. In control of apoptosis, E2F1 regulates the expression of the tumor suppressor gene Arf by binding to a non-canonical E2F binding site, within the Arf promoter, in a DP-independent manner. Furthermore, we examine the functions of E2F and DP in Drosophila melanogaster (fruit fly) to identify those mechanisms of E2F-mediated transcriptional regulation that have been evolutionarily conserved. The detailed mechanisms of how E2F protein regulates the expression of context-specific target genes will be instrumental in understanding how a single family of transcription factor regulates diverse pleiotropic cellular processes in an organism.
E2F和DP家族蛋白是高等真核生物中进化保守的转录因子。E2F和DP蛋白通常形成异二聚体复合物,通过调节生长相关基因的表达来控制细胞增殖。此外,E2F家族蛋白在各种需要表达情境特异性基因的细胞事件中发挥作用。E2F蛋白在不同的环境下使用不同的机制来调节特定环境的基因。本章的主要目的是比较哺乳动物e2f介导的控制细胞增殖、内复制和凋亡的三种不同的转录调节机制。简而言之,E2F7和E2F8通过抑制其靶基因的表达来控制内复制。他们不需要DP或pRb。在细胞凋亡的控制中,E2F1通过与Arf启动子内的非规范E2F结合位点结合,以不依赖dp的方式调节肿瘤抑制基因Arf的表达。此外,我们研究了E2F和DP在果蝇中的功能,以确定那些进化上保守的E2F介导的转录调节机制。E2F蛋白如何调控上下文特异性靶基因表达的详细机制将有助于理解单个转录因子家族如何调节生物体中多种多效性细胞过程。
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引用次数: 0
Transcriptomic Impacts of Rumen Epithelium Induced by Butyrate Infusion in Dairy Cattle in Dry Period. 丁酸盐灌注对奶牛干期瘤胃上皮转录组学的影响。
Pub Date : 2018-05-09 eCollection Date: 2018-01-01 DOI: 10.1177/1177625018774798
Ransom L Baldwin, Robert W Li, Yankai Jia, Cong-Jun Li

The purpose of this study was to evaluate the effects of butyrate infusion on rumen epithelial transcriptome. Next-generation sequencing (NGS) and bioinformatics are used to accelerate our understanding of regulation in rumen epithelial transcriptome of cattle in the dry period induced by butyrate infusion at the level of the whole transcriptome. Butyrate, as an essential element of nutrients, is a histone deacetylase (HDAC) inhibitor that can alter histone acetylation and methylation, and plays a prominent role in regulating genomic activities influencing rumen nutrition utilization and function. Ruminal infusion of butyrate was following 0-hour sampling (baseline controls) and continued for 168 hours at a rate of 5.0 L/day of a 2.5 M solution as a continuous infusion. Following the 168-hour infusion, the infusion was stopped, and cows were maintained on the basal lactation ration for an additional 168 hours for sampling. Rumen epithelial samples were serially collected via biopsy through rumen fistulae at 0-, 24-, 72-, and 168-hour (D1, D3, D7) and 168-hour post-infusion (D14). In comparison with pre-infusion at 0 hours, a total of 3513 genes were identified to be impacted in the rumen epithelium by butyrate infusion at least once at different sampling time points at a stringent cutoff of false discovery rate (FDR) < 0.01. The maximal effect of butyrate was observed at day 7. Among these impacted genes, 117 genes were responsive consistently from day 1 to day 14, and another 42 genes were lasting through day 7. Temporal effects induced by butyrate infusion indicate that the transcriptomic alterations are very dynamic. Gene ontology (GO) enrichment analysis revealed that in the early stage of rumen butyrate infusion (on day 1 and day 3 of butyrate infusion), the transcriptomic effects in the rumen epithelium were involved with mitotic cell cycle process, cell cycle process, and regulation of cell cycle. Bioinformatic analysis of cellular functions, canonical pathways, and upstream regulator of impacted genes underlie the potential mechanisms of butyrate-induced gene expression regulation in rumen epithelium. The introduction of transcriptomic and bioinformatic technologies to study nutrigenomics in the farm animal presented a new prospect to study multiple levels of biological information to better apprehend the whole animal response to nutrition, physiological state, and their interactions. The nutrigenomics approach may eventually lead to more precise management of utilization of feed resources in a more effective approach.

本研究旨在探讨丁酸盐灌注对瘤胃上皮转录组的影响。利用新一代测序技术(NGS)和生物信息学技术,在全转录组水平上加速理解丁酸盐灌注诱导干期牛瘤胃上皮转录组的调控。丁酸盐是一种能改变组蛋白乙酰化和甲基化的组蛋白去乙酰化酶(HDAC)抑制剂,是营养物质的必需元素,在调节影响瘤胃营养利用和功能的基因组活性方面发挥着重要作用。在0小时取样后(基线对照)持续瘤胃输注丁酸盐,以5.0 L/天的速率持续输注2.5 M溶液168小时。灌注168小时后,停止灌注,奶牛继续饲喂基础泌乳日粮168小时进行采样。在输注后0、24、72、168小时(D1、D3、D7)和168小时(D14),通过瘤胃瘘管连续活检收集瘤胃上皮样本。与注射前0小时相比,在严格的错误发现率(FDR)截止条件下,在不同的采样时间点至少注射一次丁酸盐,共鉴定出3513个基因在瘤胃上皮中受到影响。
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引用次数: 14
Linear-In-Flux-Expressions Methodology: Toward a Robust Mathematical Framework for Quantitative Systems Pharmacology Simulators. 线性通量表达式方法学:走向定量系统药理学模拟器的鲁棒数学框架。
Pub Date : 2017-07-26 eCollection Date: 2017-01-01 DOI: 10.1177/1177625017711414
Sean T McQuade, Ruth E Abrams, Jeffrey S Barrett, Benedetto Piccoli, Karim Azer

Quantitative Systems Pharmacology (QSP) modeling is increasingly used as a quantitative tool for advancing mechanistic hypotheses on the mechanism of action of a drug, and its pharmacological effect in relevant disease phenotypes, to enable linking the right drug to the right patient. Application of QSP models relies on creation of virtual populations for simulating scenarios of interest. Creation of virtual populations requires 2 important steps, namely, identification of a subset of model parameters that can be associated with a phenotype of disease and development of a sampling strategy from identified distributions of these parameters. We improve on existing sampling methodologies by providing a means of representing the structural relationship across model parameters and describing propagation of variability in the model. This gives a robust, systematic method for creating a virtual population. We have developed the Linear-In-Flux-Expressions (LIFE) method to simulate variability in patient pharmacokinetics and pharmacodynamics using relationships between parameters at baseline to create a virtual population. We demonstrate the importance of this methodology on a model of cholesterol metabolism. The LIFE methodology brings us a step closer toward improved QSP simulators through enhanced capture of the observed variability in drug and disease clinical data.

定量系统药理学(QSP)建模越来越多地被用作一种定量工具,用于推进药物作用机制的机制假设,及其在相关疾病表型中的药理作用,从而将正确的药物与正确的患者联系起来。QSP模型的应用依赖于创建虚拟种群来模拟感兴趣的场景。创建虚拟种群需要两个重要步骤,即确定可能与疾病表型相关的模型参数子集,并从已确定的这些参数分布中制定抽样策略。我们通过提供一种表示模型参数之间的结构关系和描述模型中可变性传播的方法来改进现有的抽样方法。这为创建虚拟人口提供了一个健壮的、系统的方法。我们开发了线性通量表达式(LIFE)方法来模拟患者药代动力学和药效学的变异性,使用基线参数之间的关系来创建虚拟人群。我们证明了这种方法对胆固醇代谢模型的重要性。LIFE方法通过增强对药物和疾病临床数据中观察到的变异性的捕获,使我们更接近于改进QSP模拟器。
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引用次数: 13
A Quantitative Systems Pharmacology Platform to Investigate the Impact of Alirocumab and Cholesterol-Lowering Therapies on Lipid Profiles and Plaque Characteristics. 研究Alirocumab和降胆固醇疗法对血脂和斑块特征影响的定量系统药理学平台。
Pub Date : 2017-06-22 eCollection Date: 2017-01-01 DOI: 10.1177/1177625017710941
Jeffrey E Ming, Ruth E Abrams, Derek W Bartlett, Mengdi Tao, Tu Nguyen, Howard Surks, Katherine Kudrycki, Ananth Kadambi, Christina M Friedrich, Nassim Djebli, Britta Goebel, Alex Koszycki, Meera Varshnaya, Joseph Elassal, Poulabi Banerjee, William J Sasiela, Michael J Reed, Jeffrey S Barrett, Karim Azer

Reduction in low-density lipoprotein cholesterol (LDL-C) is associated with decreased risk for cardiovascular disease. Alirocumab, an antibody to proprotein convertase subtilisin/kexin type 9 (PCSK9), significantly reduces LDL-C. Here, we report development of a quantitative systems pharmacology (QSP) model integrating peripheral and liver cholesterol metabolism, as well as PCSK9 function, to examine the mechanisms of action of alirocumab and other lipid-lowering therapies, including statins. The model predicts changes in LDL-C and other lipids that are consistent with effects observed in clinical trials of single or combined treatments of alirocumab and other treatments. An exploratory model to examine the effects of lipid levels on plaque dynamics was also developed. The QSP platform, on further development and qualification, may support dose optimization and clinical trial design for PCSK9 inhibitors and lipid-modulating drugs. It may also improve our understanding of factors affecting therapeutic responses in different phenotypes of dyslipidemia and cardiovascular disease.

低密度脂蛋白胆固醇(LDL-C)的降低与心血管疾病风险的降低有关。Alirocumab是一种蛋白转化酶枯草素/kexin 9型(PCSK9)抗体,可显著降低LDL-C。在这里,我们报告了一种定量系统药理学(QSP)模型的发展,该模型整合了外周和肝脏胆固醇代谢以及PCSK9功能,以检查alirocumab和其他降脂疗法(包括他汀类药物)的作用机制。该模型预测LDL-C和其他脂类的变化,与在alirocumab和其他治疗的单一或联合治疗的临床试验中观察到的效果一致。研究人员还开发了一个探索性模型来检查脂质水平对斑块动力学的影响。QSP平台的进一步开发和鉴定可能支持PCSK9抑制剂和脂质调节药物的剂量优化和临床试验设计。它也可以提高我们对影响不同表型血脂异常和心血管疾病治疗反应的因素的理解。
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引用次数: 12
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Gene regulation and systems biology
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