The role of TRPV4 in ischemic stroke

TL;DR

This paper reviews how the TRPV4 ion channel influences ischemic stroke outcomes, suggesting it could be a target for new therapies.

Contribution

The paper highlights TRPV4's phase-dependent roles in stroke pathophysiology and its potential as a mechanotherapeutic target.

Findings

TRPV4 activation during acute stroke is linked to neuronal injury and cerebral edema.

TRPV4 supports recovery by aiding arterial dilation and collateral vessel formation.

Targeting TRPV4 with physical therapies may improve stroke outcomes.

Abstract

Recent advances in mechanotransduction research have highlighted the important role of mechanosensitive ion channels, particularly the transient receptor potential vanilloid 4 (TRPV4) channel. TRPV4, a non-selective cation channel predominantly located on the plasma membrane, is widely expressed in the mammalian and human brain and exhibits sensitivity to mechanical stimuli due to its unique structural features. Emerging evidence suggests that TRPV4 may function as a modulator in the pathophysiology of ischemic stroke. During the acute phase of stroke, TRPV4 activation has been linked to neuronal injury and cerebral edema. In contrast, during the recovery phase following ischemia-reperfusion, TRPV4 appears to contribute to neurovascular remodeling by facilitating intracranial arterial dilation and collateral vessel formation. These phase-dependent roles indicate that targeted modulation of TRPV4, particularly through physical therapies, could represent a potential therapeutic strategy to improve outcomes after ischemic stroke. This review summarizes current findings on TRPV4 in stroke pathobiology and discusses its potential as a mechanotherapeutic target.

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