Lin Jun, Xiong Zhi-Gang
Department of Anesthesiology, Stony Brook University Health Sciences Center, Stony BrookNY 11794-8480, USA.
Department of Neurobiology, MRC219, Morehouse School of MedicineAtlanta, GA 30310, USA.
Int J Physiol Pathophysiol Pharmacol. 2017 Dec 25;9(6):211-216. eCollection 2017.
Ischemic stroke is a leading cause of death and long-term disabilities. The current therapy is limited to thrombolysis and mechanical recanalization, which have limited success. A better understanding of the mechanisms underlying ischemic brain injury is therefore needed for the development of more effective interventions. Glutamate receptor-mediated Ca overload and neurotoxicity have been well established for decades. However, clinical trials failed to show a satisfactory effect with the antagonists of glutamate receptors. Other glutamate-independent mechanisms, such as activation of acid-sensing ion channels and transient receptor potential melastatin 7 (TRPM7), have recently emerged as important events responsible for neuronal injury under ischemic conditions. In this review, we discuss how TRPM7 channels participate in ischemic brain injury.
缺血性中风是导致死亡和长期残疾的主要原因。目前的治疗方法仅限于溶栓和机械再通，效果有限。因此，为了开发更有效的干预措施，需要更好地了解缺血性脑损伤的潜在机制。几十年来，谷氨酸受体介导的钙超载和神经毒性已得到充分证实。然而，临床试验未能显示谷氨酸受体拮抗剂有令人满意的效果。其他不依赖谷氨酸的机制，如酸敏感离子通道的激活和瞬时受体电位香草酸亚型7（TRPM7），最近已成为缺血条件下导致神经元损伤的重要因素。在这篇综述中，我们讨论了TRPM7通道如何参与缺血性脑损伤。
