ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
TRPV4/IP3R-1-mediated endothelial pyroptosis drives pulmonary microvascular endothelial permeability in endotoxin-induced acute lung injury.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSepsis-induced acute lung injury (ALI) is characterized by edema resulting from increased vascular permeability. Transient receptor potential vanilloid 4 (TRPV4) interacts with inositol 1,4,5-trisphosphate receptor type 1 (IP3R-1) through calmodulin-binding domains and regulates vascular permeability. However, the specific mechanisms underlying the roles of TRPV4 and IP3R-1 in endothelial pyroptosis and vascular permeability remain unclear.
methodsEMPs were measured in septic patients and controls, and co-cultured with human pulmonary microvascular endothelial cells (HPMECs). LPS-induced ALI was assessed in wild-type or Gsdmd
resultsElevated EMPs in septic patients enhanced endothelial permeability, upregulated TRPV4 and GSDMD-NT generation in HPMECs. TRPV4 promotes HPMECs permeability and pyroptosis in an IP3R-1-dependent manner. TRPV4 inhibition attenuated lung injury and ameliorated pulmonary dysfunction, while Trpv4 knockdown improved survival. Knockdown of IP3R-1 reduced intracellular Ca
conclusionsTRPV4 disrupts HPMEC integrity via IP3R-1 and triggers GSDMD-mediated pyroptosis through a Ca
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