NIH R01 · 2024
REGULATION OF THE MACROPHAGE INFLAMMATORY PHENOTYPE IN ARDS
Our published data show that genetic ablation and pharmacologic inhibition of NFATc3 in macrophages is beneficial in maintaining alveolar-capillary barrier function, prevents inflammatory cytokine release and neutrophilic inflammation, improved arterial oxygenation and survival in the LPS and cecal ligation puncture mouse models of ARDS. Here, we propose to determine the granular details of the downstream molecular targets of NFATc3 using a 2-hit mouse model, human lung macrophages, and BALF from patients with ARDS. Our team has developed a novel non-toxic cell permeable calcineurin inhibitory (CNI) peptide (CNI103) that blocks activation of NFATc3 in macrophages and mitigates ARDS in mice.…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.