视网膜神经元细胞是视觉形成的重要参与者。由于再生能力差,当神经元细胞发生损伤或死亡时,往往会导致视功能不可逆转的损害。P2X7受体是一种三磷酸腺苷(ATP)门控的阳离子通道受体。近期研究发现,P2X7受体在视网膜神经元细胞的变性死亡中发挥着重要的作用。在一系列动物模型中,暴露于缺血缺氧、高眼压、机械创伤等环境或加入外源性受体激动剂的情况下,胞外升高的ATP可活化神经元细胞表面的P2X7受体。而经活化的受体可经直接或间接途径引起神经节细胞、光感受器细胞等视网膜神经元细胞的死亡,通过受体特异性的拮抗剂及基因敲除技术下调P2X7受体的表达及功能后,神经元细胞的丢失得到了明显的改善。P2X7受体有可能成为与神经元细胞损伤相关的视网膜疾病的一个新的治疗靶点。
Retinal neuronal cells are crucial in the formation of vision. Injury or death of these cells may lead to irreversible damage to visual function due to their low regenerative capacity. The P2X7 receptor is a trimeric adenosine triphosphate (ATP)-gated cation channel. Recent studies have shown that P2X7 receptor plays a role in retinal neuronal death. In a series of animal models, when exposed to conditions of hypoxia or ischemia, elevated ocular pressure, trauma and exogenous agonists, P2X7 receptor activated by extracellular ATP can cause death of retinal neuronal cells such as retinal ganglion cells and photoreceptor cells through direct or indirect pathways. Blocking the expression and function of P2X7 receptor by its specific antagonist and gene knocking-out, the loss of retinal neuronal cells is significantly attenuated. P2X7 receptor may become a potential novel neuroprotective target for diseases related to the loss of retinal neurons.