TRP Channels in Stroke

被引:2
作者
Zong, Pengyu [1 ,2 ]
Li, Cindy X. [1 ]
Feng, Jianlin [1 ]
Cicchetti, Mara [1 ,3 ]
Yue, Lixia [1 ]
机构
[1] Univ Connecticut, Calhoun Cardiol Ctr, Dept Cell Biol, Sch Med,UConn Hlth, Farmington, CT 06030 USA
[2] Univ Connecticut, Connecticut Inst Brain & Cognit Sci, Unit 1272, 337 Mansfield Rd, Storrs, CT 06269 USA
[3] Univ Pittsburgh, Dept Neurosci, 4200 Fifth Ave, Pittsburgh, PA 15260 USA
关键词
Stroke; TRP channels; Neuronal death; Immune cell infiltration; Blood-brain barrier; Glial activation; RECEPTOR POTENTIAL CHANNELS; MELASTATIN; 2; TRPM2; CATION CHANNEL; ION-CHANNEL; OLMSTED SYNDROME; ISCHEMIC-STROKE; CA2+ CHANNEL; FUNCTIONAL-CHARACTERIZATION; NEUTROPHIL ACTIVATION; CAPSAICIN RECEPTOR;
D O I
10.1007/s12264-023-01151-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Ischemic stroke is a devastating disease that affects millions of patients worldwide. Unfortunately, there are no effective medications for mitigating brain injury after ischemic stroke. TRP channels are evolutionally ancient biosensors that detect external stimuli as well as tissue or cellular injury. To date, many members of the TRP superfamily have been reported to contribute to ischemic brain injury, including the TRPC subfamily (1, 3, 4, 5, 6, 7), TRPV subfamily (1, 2, 3, 4) and TRPM subfamily (2, 4, 7). These TRP channels share structural similarities but have distinct channel functions and properties. Their activation during ischemic stroke can be beneficial, detrimental, or even both. In this review, we focus on discussing the interesting features of stroke-related TRP channels and summarizing the underlying cellular and molecular mechanisms responsible for their involvement in ischemic brain injury.
引用
收藏
页码:1141 / 1159
页数:19
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