Loss of TRPV4 is insufficient to promote repair in a spinal cord injury contusion model.

ABSTRACT: Microglia, the primary phagocytes activated after spinal cord injury (SCI), play a key role in containing the lesion and protecting the glial scar from infiltrating immune cells. Although these responses are initially protective, excessive microglial proliferation and sustained pro-inflammatory activation can worsen secondary damage and limit recovery. Modulating microglial activity has been proposed as a potential therapeutic approach to enhance SCI repair. Previous studies suggest that constitutive loss of the mechanosensory channel TRPV4 (transient receptor potential vanilloid 4) reduces microgliosis and inflammation at the lesion site, improving functional outcomes. TRPV4 is a Ca²⁺-permeable channel implicated in several microglial characteristics, like morphology, motility,

SUBMITTER: Mertens M 

PROVIDER: S-EPMC12287530 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature