Nogo-B impairs efferocytosis in monocyte-derived macrophages and exacerbates septic liver injury

Efferocytosis is compromised during sepsis, contributing to enhanced inflammation and organ damage. Our study identified Nogo-B as a critical mediator linking disrupted mitochondrial calcium uptake to impaired MDM efferocytosis. Targeting Nogo-B may represent a novel therapeutic strategy to restore efferocytosis and attenuate sepsis-related tissue injury. Further translational studies are needed to validate these findings in human disease.