Brain and cancer: The protective role of erythropoietin

Brain and cancer: The protective role of erythropoietin
复制标题

DOI:
10.1002/med.20012
复制
发表时间:
2005-03-01
影响因子:
13.3
通讯作者:
Grasso, G
Grasso, G
中科院分区:
医学1区
文献类型:
--
作者:
Buemi, M;Caccamo, C;Grasso, G

文献摘要

被引文献

相似文献

促红细胞生成素(Epo)是一种多效性药物,也就是说,它可以以不同的方式作用于多种细胞类型。在脑内发现了一个独立的Epo/Epo受体系统(EpoR),推测该激素可能参与脑功能。Epo/EpoR表达在个体发育过程中发生变化,从而表明该系统在神经发育中的重要性。此外,缺氧诱导的成年脑中Epo的产生表明,在脑损伤的情况下,它可以发挥神经营养和神经保护作用。Epo还可影响神经传递,诱导神经递质(NT)的释放。由于促红细胞生成素可能作为一种生长因子和血管生成因子,其在贫血癌症患者中的治疗仍是一个有争议的问题。在我们的推测性假设中,Epo可能参与了一个“两步过程”,在新血管形成阶段之后,导致其下调。此外,Epo激活的信号通路可以作为干扰肿瘤细胞周期的可能靶点。总之,用rHuEpo治疗可以改变不同病理条件下的治疗观点。如中枢神经系统(CNS)疾病,但需要进一步研究以阐明其在不同临床领域的生理病理学活性。(C)2004 Wiley Periodicals,Inc. Med Res Rev,25,No.2,245 -259,2005。
Erythropoietin (Epo) is a pleiotropic agent, that is to say, it can act on several cell types in different ways. An independent system Epo/Epo receptor (EpoR) was detected in brain, leading to the hypothesis that this hormone could be involved in cerebral functions. Epo/EpoR expression changes during ontogenesis, thus indicating the importance of this system in neurodevelopment. Moreover, the hypoxia-induced production of Epo in the adult brain suggests that it could exert a neurotrophic and neuroprotective effect in case of brain injury. Epo could also influence neurotransmission, inducing neurotransmitters (NT) release. Epo therapy in anemic cancer patients is still a controversial issue, because of its possible action as a growth and an angiogenic factor. In our speculative hypothesis Epo could be involved in a "two steps process" that, after a neovascularization phase, leads to its down regulation. Moreover, Epo-activated signaling pathways could be modulated as possible targets to interfere in neoplastic cells cycle. In conclusion, treatment with rHuEpo could change therapeutical perspectives in different pathological conditions. such as central nervous system (CNS) diseases, but further studies are needed to clarify its physiopathological activities in different clinical fields. (C) 2004 Wiley Periodicals, Inc. Med Res Rev, 25, No.2,245-259, 2005.