Pengyu Zong1,2 · Cindy X. Li1 · Jianlin Feng1 · Mara Cicchetti1,3 · Lixia Yue11 Department of Cell Biology, Calhoun Cardiology Center, School of Medicine (UConn Health), University of Connecticut, Farmington, CT 06030, USA
2 Institute for the Brain and Cognitive Sciences, University of Connecticut, 337 Mansfeld Road, Unit 1272, Storrs, CT 06269, USA
3 Present Address: Department of Neuroscience, University of Pittsburgh, 4200 Fifth Ave, Pittsburgh, PA 15260, USA
Abstract
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.
Keywords
Stroke; TRP channels; Neuronal death; Immune cell infltration; Blood-brain barrier; Glial activation
