Department of Biology, University of Miami, 1301 Memorial Drive, Coral Gables, FL 33146, United States of America.
Department of Biology, University of Miami, 1301 Memorial Drive, Coral Gables, FL 33146, United States of America.
Exp Neurol. 2020 Jan;323:113090. doi: 10.1016/j.expneurol.2019.113090. Epub 2019 Oct 25.
Non-mammalian models of CIPN remain relatively sparse, but the knowledge gained from the few published studies suggest that these species have great potential to serve as a discovery platform for new pathways and underlying genetic mechanisms of CIPN. These models permit large-scale genetic and pharmacological screening, and they are highly suitable for in vivo imaging. CIPN phenotypes described in rodents have been confirmed in those models, and conversely, genetic players leading to axon de- and regeneration under conditions of chemotherapy treatment identified in these non-mammalian species have been validated in rodents. Given the need for non-traditional approaches with which to identify new CIPN mechanisms, these models bear a strong potential due to the conservation of basic mechanisms by which chemotherapeutic agents induce neurotoxicity.
非哺乳动物的 CIPN 模型仍然相对较少,但从少数已发表的研究中获得的知识表明,这些物种具有很大的潜力成为 CIPN 的新途径和潜在遗传机制的发现平台。这些模型允许进行大规模的遗传和药理学筛选,并且非常适合体内成像。在啮齿动物中描述的 CIPN 表型已在这些模型中得到证实,反之亦然,在这些非哺乳动物中确定的导致化疗治疗条件下轴突去再生的遗传因子在啮齿动物中得到了验证。鉴于需要采用非传统方法来识别新的 CIPN 机制,这些模型具有很强的潜力,因为化学治疗剂诱导神经毒性的基本机制是保守的。