Another win for mimetic peptides in stroke: Disruption of TRPM2-NMDAR signaling

Andrew K J Boyce; Roger J Thompson

doi:10.1016/j.neuron.2022.05.020

Another win for mimetic peptides in stroke: Disruption of TRPM2-NMDAR signaling

Neuron. 2022 Jun 15;110(12):1881-1884. doi: 10.1016/j.neuron.2022.05.020.

Authors

Andrew K J Boyce¹, Roger J Thompson²

Affiliations

¹ Department of Cell Biology and Anatomy, Hotchkiss Brain Institute, University of Calgary, Calgary, AB T2N4N1, Canada.
² Department of Cell Biology and Anatomy, Hotchkiss Brain Institute, University of Calgary, Calgary, AB T2N4N1, Canada. Electronic address: thompsrj@ucalgary.ca.

PMID: 35709691
DOI: 10.1016/j.neuron.2022.05.020

Abstract

Glutamate excitotoxicity during ischemia triggers an intracellular signaling avalanche leading to cell death, yet blocking NMDA receptors directly in human stroke trials failed. In this issue of Neuron, Zong et al. (2022) disrupt downstream NMDAR-TRPM2 coupling to improve stroke outcomes, supporting intracellular NMDAR signaling as an alternate therapeutic target.

Publication types

Comment

MeSH terms

Humans
Neurons / metabolism
Peptides / metabolism
Receptors, N-Methyl-D-Aspartate / metabolism
Stroke* / drug therapy
TRPM Cation Channels* / metabolism

Substances

Peptides
Receptors, N-Methyl-D-Aspartate
TRPM Cation Channels
TRPM2 protein, human