Integrated transcriptomic and weighted gene co-expression network analyses identify the UCHL1-MUCL1 axis as a key regulator of endothelial dysfunction in sepsis

The UCHL1-MUCL1 axis promoted sepsis-induced endothelial inflammation and apoptosis through the regulation of the β-catenin/NF-κB pathway. Targeting MUCL1 or its regulator UCHL1 may represent a promising therapeutic strategy to mitigate vascular endothelial dysfunction in sepsis.