Towards bridging the translational gap by improved modeling of human nociception in health and disease.

Maximilian Zeidler, Kai K Kummer, Michaela Kress
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Abstract

Despite numerous studies which have explored the pathogenesis of pain disorders in preclinical models, there is a pronounced translational gap, which is at least partially caused by differences between the human and rodent nociceptive system. An elegant way to bridge this divide is the exploitation of human-induced pluripotent stem cell (iPSC) reprogramming into human iPSC-derived nociceptors (iDNs). Several protocols were developed and optimized to model nociceptive processes in health and disease. Here we provide an overview of the different approaches and summarize the knowledge obtained from such models on pain pathologies associated with monogenetic sensory disorders so far. In addition, novel perspectives offered by increasing the complexity of the model systems further to better reflect the natural environment of nociceptive neurons by involving other cell types in 3D model systems are described.

通过改进健康和疾病中人类痛觉的建模,缩小转化差距。
尽管已有大量研究探索了临床前模型中疼痛疾病的发病机理,但仍存在明显的转化差距,这至少部分是由人类和啮齿动物痛觉系统之间的差异造成的。弥合这一鸿沟的一个有效方法是利用人类诱导多能干细胞(iPSC)重编程,将其转化为源自人类 iPSC 的痛觉感受器(iDNs)。人们开发并优化了几种方案,以模拟健康和疾病中的痛觉过程。在此,我们概述了不同的方法,并总结了迄今为止从此类模型中获得的与单基因感觉障碍相关的疼痛病理知识。此外,我们还介绍了通过在三维模型系统中加入其他细胞类型,进一步提高模型系统的复杂性以更好地反映痛觉神经元的自然环境所带来的新视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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