Ischemic stroke is one of the leading causes of death and disability worldwide. Currently, there are few drugs available for treatment of ischemic stroke, and the lack of high-quality targets has severely restricted the development of innovative drugs. Glial cells play crucial roles in the pathophysiological process of ischemic stroke, particularly through the regulation of the inflammatory response and immunomodulation. Transient receptor potential (TRP) channels, as a crucial class of membrane proteins, are sensors for a variety of cellular and environmental signals in the central nervous system. Accumulating evidence indicates that alterations in the expression and function of TRP channels in glial cells significantly regulate the onset and progression of ischemic stroke. Notably, pharmacological inhibition or genetic knockout of specific TRP channels can effectively alleviate ischemic stroke-induced neuronal damage, highlighting their potential as therapeutic targets. We summarize and discuss the molecular and cellular mechanisms of TRP channels regulation in glial cells during ischemic stroke, as well as the mechanisms of neuroprotective agents targeting TRP channels. Furthermore, we propose a series of recommendations for future experiments aimed at developing neuroprotective drugs for ischemic stroke by targeting TRP channels.
Zheng et al. (Wed,) studied this question.