Lencesova Lubomira, Krizanova Olga
Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Gen Physiol Biophys. 2012 Jun;31(2):119-30. doi: 10.4149/gpb_2012_014.
Inositol 1,4,5-trisphosphate (IP3) receptors are intracellular calcium channels that are able to release calcium from intracellular stores upon activation by IP3 and modulation by calcium. IP3 receptors are involved in variety of processes during physiological, but also in the pathophysiological states. Unraveling their regulation and function, especially under the pathological situations can result in a development of new therapeutic strategies based on the IP3 receptor´s activation and/or blocking. To the stimuli that can modulate IP3 receptors belong several stress factors (e.g. immobilization stress, oxidative stress and hypoxia) and also apoptosis. Depending on the length and strength of the stress stimulus, expression of IP3 receptors can be increased, or decreased. Therefore, in this minireview modulation of IP3 receptors by some stressors is discussed. Since it was already shown that strong hypoxia might lead to the apoptosis induction, special focus will be given to the hypoxic stress and induction of apoptosis.
肌醇1,4,5 -三磷酸（IP3）受体是细胞内钙通道，在被IP3激活并受钙调节后，能够从细胞内储存库释放钙。IP3受体在生理过程中以及病理生理状态下都参与多种过程。阐明它们的调节和功能，尤其是在病理情况下，可能会基于IP3受体的激活和/或阻断开发出新的治疗策略。能够调节IP3受体的刺激因素包括多种应激因素（如制动应激、氧化应激和缺氧）以及细胞凋亡。根据应激刺激的时长和强度，IP3受体的表达可能会增加或减少。因此，在本综述中讨论了一些应激源对IP3受体的调节作用。由于已经表明强烈的缺氧可能导致细胞凋亡诱导，因此将特别关注缺氧应激和细胞凋亡诱导。
