Inhibition of TRPV4 attenuates ferroptosis against LPS-induced ALI via Ca2+ pathway

Acute lung injury (ALI) is an inflammation of the lungs with high incidence rate and mortality. Ferroptosis a new cell death, which has influence in body organs. Transient receptor potential vanillin-4 (TRPV4) channel key mediator Ca2+, its activation induces ferroptosis. The purpose study to investigate function TRPV4 on ferroptosis ALI mice induced by lipopolysaccharide (LPS). In vitro, regulation Ca2+ was detected CCK-8, fluorescent probe, western blot BEAS-2B cells. vivo, role antagonists analyzed determination pulmonary inflammation, edema, ALI. expression intracellular concentration were up-regulated ALI, antagonist suppressed LPS-induced cells, including decreased MDA ROS levels, increased GPX4 protein level viability. showed activated compared control group, administration inhibition had protective effects mice, improving pathological characteristics, reducing degree results manifested that mediated might moderate damage suppressing