Faiq Muneeb A, Sidhu Talvir, Sofi Rayees A, Singh Himanshu N, Qadri Rizwana, Dada Rima, Bhartiya Shibal, Gagrani Meghal, Dada Tanuj
Dr Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India.
J&K Health Services Department, Srinagar, Jammu and Kashmir, India.
J Curr Glaucoma Pract. 2019 Jan-Apr;13(1):3-8. doi: 10.5005/jp-journals-10078-1241.
Conventional experimental approaches to understand glaucoma etiology and pathogenesis and, consequently, predict its course of progression have not seen much success due to the involvement of numerous molecular, cellular, and other moieties. An overwhelming number of these moieties at different levels combined with numerous environmental factors further complicate the intricacy. Interaction patterns between these factors are important to understand yet difficult to probe with conservative experimental approaches.
We performed a system-level analysis with mathematical modeling by developing and analyzing rate equations with respect to the cellular events in glaucoma pathogenesis. Twenty-two events were enlisted from the literature survey and were analyzed in terms of the sensitivity coefficient of retinal ganglion cells. A separate rate equation was developed for cellular stress also. The results were analyzed with respect to time, and the time course of the events with respect to various cellular moieties was analyzed.
Our results suggest that microglia activation is among the earliest events in glaucoma pathogenesis. This modeling method yields a wealth of useful information which may serve as an important guide to better understand glaucoma pathogenesis and design experimental approaches and also identify useful diagnostic/predictive methods and important therapeutic targets.
We here report the first mathematical model for glaucoma pathogenesis which provides important insight into the sensitivity coefficient and glia-mediated pathology of glaucoma.
Faiq MA, Sidhu T, A Novel Mathematical Model of Glaucoma Pathogenesis. J Curr Glaucoma Pract 2019; 13(1):3-8.
由于青光眼病因和发病机制涉及众多分子、细胞及其他部分，传统的用于理解其病因和发病机制并进而预测其进展过程的实验方法并未取得显著成功。不同层面上数量众多的这些部分，再加上众多环境因素，使得复杂性进一步增加。这些因素之间的相互作用模式虽对理解很重要，但用传统实验方法却难以探究。
我们通过开发和分析与青光眼发病机制中的细胞事件相关的速率方程，进行了系统层面的数学建模分析。从文献调研中列出了22个事件，并根据视网膜神经节细胞的敏感性系数进行分析。还为细胞应激单独开发了一个速率方程。对结果进行了时间方面的分析，并分析了各细胞部分相关事件的时间进程。
我们的结果表明，小胶质细胞激活是青光眼发病机制中最早出现的事件之一。这种建模方法产生了大量有用信息，可作为更好理解青光眼发病机制、设计实验方法以及识别有用的诊断/预测方法和重要治疗靶点的重要指南。
我们在此报告首个青光眼发病机制的数学模型，该模型为青光眼的敏感性系数和胶质细胞介导的病理提供了重要见解。
Faiq MA, Sidhu T, 青光眼发病机制的一种新型数学模型。《当代青光眼实践杂志》2019年；13(1):3 - 8。
