TRPV4, short for transient receptor potential channel subfamily V member 4, is a polymodal, nonselective, calcium-permeant cation channel. It is activated by both endogenous and exogenous stimuli, participating in numerous physiological and pathophysiological processes. TRPV4-expressing cells include both neuronal and non-neuronal ones, responding to various biochemical and biomechanical stimuli [1,2].

In macrophages, TRPV4 plays a crucial role in multiple inflammatory conditions. Deletion of TRPV4 in macrophages suppresses allergic and non-allergic itch in a mouse model, suggesting its role in skin disease [1]. In sepsis-induced lung injury, TRPV4-knockout in macrophages impacts glucose uptake through GLUT1, phagolysosome maturation, and ultimately limits sepsis-induced lung injury [3].

In conclusion, TRPV4 is essential in various biological processes, especially in the context of inflammation and immunity. The use of TRPV4-knockout mouse models has revealed its role in diseases such as skin diseases and sepsis-induced lung injury, providing valuable insights into the mechanisms underlying these diseases and potential therapeutic targets.