Therapeutic targeting of endothelial calcium signaling accelerates the resolution of lung injury.

ABSTRACT: Acute respiratory distress syndrome (ARDS) is a severe pulmonary disease characterized by acute, noncardiogenic pulmonary edema and hypoxemia leading to respiratory failure. It is induced by a diverse array of etiologies, including recent SARS-CoV-2 infection. The current standard of care for ARDS remains predominantly supportive, underscoring the urgent need for targeted pharmacological interventions. To address this critical gap, we developed an inhibitor of the microtubule accessory factor end-binding protein 3 (EB3), a key mediator of pathological calcium signaling in endothelial cells. During injury, EB3 facilitates inositol 1,4,5-trisphosphate receptor 3 (IP₃R3) clustering on the endoplasmic reticulum membrane, activating widespread calcium release from intracellular store

SUBMITTER: Chan WC 

PROVIDER: S-EPMC12627862 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature