FIGURE 4.

Schematic of the potential role of transient receptor potential vanilloid 4 (TRPV4) inhibition in limiting neurological injury. (A) In injured neurons, activation of TRPV4 and RhoA leads to ROCK-dependent bundling of actin at the base of the axonal growth cone, thereby restricting microtubule entry into the growth cone. (B) Inhibition of TRPV4 could potentially reduce RhoA activation and create a regeneration-permissive environment within the axonal growth cone. Specific TRPV4–RhoA functions in glia require further study. (C) In injured vascular endothelial cells of the brain and spinal cord, TRPV4 activation leads to RhoA-dependent disruption of the blood–brain barrier with subsequent extravasation of blood constituents and inflammatory cells, which worsen local tissue injury. (D) Inhibition of TRPV4 could potentially reduce RhoA-dependent blood–brain barrier breakdown, thereby limiting the extent of surrounding tissue injury