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Calcium, a multitasking signaling actor in airway smooth muscle cells, as a target of novel strategies to limit airway disease?

机译:钙是气道平滑肌细胞中的一种多任务信号转导因子,是限制气道疾病的新策略的靶标吗?

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Asthma, Chronic Obstructive Pulmonary Disease (COPD),… words that have entered our everyday vocabulary, but more especially diseases whose prevalence is growing steadily and which faithfully illustrate the continuous increase in respiratory diseases. The quantified estimations, suggesting that asthma affects 300,000 persons worldwide and that COPD will become the third cause of death in 2020, give a very clear vision of the future of these diseases. Thus, the investigation of the cellular mechanisms of the functioning of the respiratory system has led to the identification of signaling pathways in which modifications could be responsible for the appearance of pathophysiological situations. The ubiquitous nature of the role of calcium as a signaling actor in smooth muscle cells (SMC) associated with the fact that the SMC are major constituents of the airways, are two basic findings that clearly justify the importance of this book edited by Yong-Xiao Wang. Thus, the union of the 25 articles by almost 50 contributors that make up the 460 pages of this book clearly illustrates the variety and importance of the role of calcium in airway SMC (ASMC). However, more than a simple illustration, this book is a form of “state of the art” of the role of calcium in the physiology of ASMC and then, in its potential involvement in various pathophysiological conditions. However, it is first necessary to recognize the importance of Yong-Xiao Wang, who has gathered contributors recognized as experts in the field. The numerous works published by Yong-Xiao Wang on this subject therefore confer him the legitimacy to be the editor of such a book based on a simple observation: the number of scientific research is steadily increasing without a “ comprehensive book compiling and detailing the (our) state-of-the-art advances ” (preface p. v) is available. One reason for this increased interest in the role of calcium in ASCM directly comes from the involvement of alterations in regulating the calcium movements in pathophysiological situations. In this context, although the findings presented by Anderson in 1983 in one of the 1st review available on this subject seem very distant, he was clearly establishing the basis for all work presented here: “ It cannot be excluded that changes in one or more of these mechanisms, induced by mediators, hormones, or other agents may be a contribution factor to airway hyperreactivity ” (Anderson, 1983 ). Therefore, in the context of recent data collection on this theme, a book review on “ calcium signaling in airway smooth muscle cells ” should probably aim to try to offer an overview of this subject. As mention above, since this book is clearly a state of the art in the field, it seems to me that a figure summarizing the physiological pathways involving calcium in SMC could be the main asset that a short “book review” can provide (Figure 1 ). It will enable readers to get an overview of the calcium-dependent pathways that are targets to consider in pathophysiological situations. Figure 1 Calcium-dependent pathways in airways smooth muscle cells . This figure summarizes the main effects of intracellular calcium dynamics (Ca~(2+)-Sparks/Oscillations) from calcium entry into cell and local Calcium-Induced Calcium-Release (CICR) resulting from Endoplasmic Reticulum (ER) protein (RYR, Ryanodine Receptor; IP3R, inositol triphosphate Receptor) activation. The numbers in black circles refer to the following chapters of the book: 1, Mei et al. (pp. 3–20); 2, Kume (pp. 51–83); 3, Gallos et al. (pp. 86–106); 4, Liu et al. (pp. 109–124); 5, Delmotte et al. (pp. 211–234); 6, Pabelick et al. (pp. 235–246); 7, Ito (pp. 287–307); 8, Tran and Teoh (pp. 310–320); 9, Song et al. (pp. 393–407). Figure 1 shows the intracellular mechanisms involving the calcium in the operation of the ASCM. The main roles presented here show the involvement of calcium in the control of the contraction and relaxation of ASCM but also its role in the control of cell proliferation. Although the main calcium-dependent pathways in ASMC are recalled in Figure 1 , they can be modulated by sex hormones or maturation as well-described by Y.S. Prakash et al. in two chapters (pp. 322–332; 333–357). Moreover, since the respiratory pathologies are unanimously recognized as associated with inflammatory situations, the three chapters describing the influence of inflammatory mediators (H. Matsumoto pp. 359–379; Y. Amrani pp. 423–439; Y. Su pp. 441–457) on Ca-dependent pathways in ASMC perfectly complement this book. Finally this synthesis can be well-completed by the two chapters presenting an interesting approach based on mathematical simulation of calcium oscillation in the SMC. Therefore, the mathematical models of calcium dynamics proposed by Sneyd et al. (pp. 341–357) have to be related with the observations of E. Roux (pp. 147–175) on the kinetics of the mechanisms involved in calcium homeodynamics. In conclusion by drawing an updated synthesis o
机译:哮喘,慢性阻塞性肺疾病(COPD),……已经进入我们的日常词汇,尤其是其流行率稳定增长且忠实地说明呼吸系统疾病持续增加的疾病。量化估计表明,哮喘影响了全世界30万人,而COPD将在2020年成为第三大死亡原因,这使人们对这些疾病的未来有了清晰的认识。因此,对呼吸系统功能的细胞机制的研究导致了信号通路的鉴定,其中的修饰可能是病理生理情况的出现原因。钙在平滑肌细胞(SMC)中作为信号转导因子的作用无处不在,与SMC是气道的主要成分这一事实有关,这是两个基本发现,清楚地证明了Yong-Xiao编辑的这本书的重要性王因此,构成本书460页的近50位贡献者的25篇文章的结合清楚地说明了钙在气道SMC(ASMC)中的作用的多样性和重要性。然而,这本书不仅仅是一个简单的例子,更是钙在ASMC生理学中的作用的“最新技术”形式,然后是钙在各种病理生理状况中的潜在作用。但是,首先有必要认识到王永孝的重要性,他聚集了被认为是该领域专家的贡献者。因此,基于简单的观察,王永孝出版的有关该主题的大量著作赋予他成为该书的编辑者的合法性:科学研究的数量稳步增加,而无需编写“全面的书”。 )(最新的进展)。人们对钙在ASCM中的作用越来越感兴趣的一个原因直接来自在病理生理情况下改变参与调节钙运动。在这种情况下,尽管安德森(Anderson)于1983年在有关该主题的第一篇评论中提出的发现似乎相去甚远,但他显然正在为此处提出的所有工作奠定基础:“不能排除的是,一个或多个这些由介体,激素或其他因子诱导的机制可能是气道反应过度的贡献因素”(安德森,1983年)。因此,在有关该主题的最新数据收集的背景下,有关“气道平滑肌细胞中钙信号传导”的书评应该旨在试图对该主题进行概述。如上所述,由于这本书显然是该领域的最新技术,在我看来,总结SMC中涉及钙的生理途径的数字可能是简短的“书评”可以提供的主要资产(图1)。 )。它将使读者能够大致了解钙依赖的途径,这些途径是病理生理情况下要考虑的目标。图1气道平滑肌细胞中的钙依赖途径。该图总结了钙进入细胞以及局部内质网蛋白(ER)(RYR,Ryanodine)引起的局部钙诱导钙释放酶(CICR)引起的细胞内钙动力学(Ca〜(2 +)-Sparks / Oscillations)的主要作用。受体; IP3R,三磷酸肌醇受体)激活。黑色圆圈中的数字表示该书的以下章节:1,Mei等。 (第3-20页); 2,久米(第51–83页); 3,Gallos等。 (第86-106页); 4,刘等。 (第109-124页); 5,Delmotte等。 (第211-234页); 6,Pabelick等。 (第235-246页);伊藤7(第287-307页); 8,Tran和Teoh(pp。310-320); 9,Song等。 (第393-407页)。图1显示了ASCM运作中涉及钙的细胞内机制。此处介绍的主要作用表明钙参与了ASCM的收缩和舒张控制,还涉及了钙在细胞增殖控制中的作用。尽管图1中回忆了ASMC中主要的钙依赖性途径,但它们可以通过性激素或成熟来调节,正如Y.S. Prakash等。分两章(第322-332页; 333-357页)。此外,由于一致认为呼吸道病理与炎症状况有关,因此三章描述了炎症介质的影响(H. Matsumoto pp。359-379; Y。Amrani pp。423-439; Y。Su pp。441- 457)对ASMC中Ca依赖的途径进行了完美的补充。最后,这两章可以很好地完成该合成,这两个章节基于SMC中钙振荡的数学模拟提出了一种有趣的方法。因此,Sneyd等人提出了钙动力学的数学模型。 (第341–357页)必须与鲁克斯(E. Roux)(第147–175页)的钙动力学相关机理的动力学相关。最后通过绘制更新的综合

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