USP7 promotes endothelial activation to aggravate sepsis-induced acute lung injury through PDK1/AKT/NF-κB signaling pathway.

ABSTRACT: Disruption of the endothelial cell barrier and the subsequent inflammatory response represent a central pathological feature of acute lung injury (ALI). Ubiquitination plays a pivotal role in regulating protein stability, intracellular transport, and enzyme activity, which is typically reversed by deubiquitinating enzymes. Nevertheless, the function of deubiquitinating enzymes in endothelial biology and in ALI remains largely uninvestigated. The present study demonstrates that the expression of USP7 is increased in instances of endothelial inflammation and ALI. The knockdown or inhibition of USP7 using specific inhibitors was observed to significantly reduce the TNF-α-induced inflammatory response of endothelial cells and their adhesion capacity to monocytes. Conversely, the overexpression

SUBMITTER: Liu Z 

PROVIDER: S-EPMC12006344 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature