Yun J K, McCormick T S, Judware R, Lapetina E G
Molecular Cardiovascular Research Center, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.
Neurochem Res. 1997 Apr;22(4):517-21. doi: 10.1023/a:1027328314968.
Oxygen plays such a critical role in the central nervous system that a specialized mechanism of oxygen delivery to neurons is required. Reduced oxygen tension, or hypoxia, may have severe detrimental effects on neuronal cells. Several studies suggest that hypoxia can induce cellular adaptive responses that overcome apoptotic signals in order to minimize hypoxic injury or damage. Adaptive responses of neuronal cells to hypoxia may involve activation of various ion channels, as well as induction of specific gene expression. For example, ATP sensitive K+ channels are activated by hypoxia in selective neuronal cells, and may play a role in cell survival during hypoxia/anoxia. Additionally, hypoxia-induced c-Jun, bFGF and NGF expression appear to be associated with prevention (or delay) of neuronal cell apoptosis. In this paper, these adaptive responses to hypoxia in neuronal cells are discussed to examine the possible role of hypoxia in pathophysiology of diseases.
氧气在中枢神经系统中起着至关重要的作用,因此需要一种专门的向神经元输送氧气的机制。氧分压降低,即缺氧,可能会对神经元细胞产生严重的有害影响。多项研究表明,缺氧可诱导细胞适应性反应,以克服凋亡信号,从而将缺氧损伤降至最低。神经元细胞对缺氧的适应性反应可能涉及各种离子通道的激活,以及特定基因表达的诱导。例如,ATP敏感性钾通道在选择性神经元细胞中被缺氧激活,可能在缺氧/无氧期间的细胞存活中发挥作用。此外,缺氧诱导的c-Jun、bFGF和NGF表达似乎与预防(或延迟)神经元细胞凋亡有关。本文讨论了神经元细胞对缺氧的这些适应性反应,以探讨缺氧在疾病病理生理学中的可能作用。