Ontology highlight
ABSTRACT: Objective
A cardiovascular safety issue has been associated with JAK inhibitors (JAKi). This study compares the effects of distinct approved JAKi on endothelial cell (EC) dysfunction and apoptosis during inflammation.Methods
Massive inflammation was induced in human vascular ECs by tumor necrosis factor (TNF) with interleukin-17A (IL-17A) treated or not treated with tofacitinib, baricitinib, upadacitinib, peficitinib, ruxolitinib, and fedratinib at 1 or 10 μM. Levels of IL-6 and IL-8 were measured by enzyme-linked immunosorbent assay. Variations in gene expression of adhesion molecules and factors of blood coagulation and fibrinolysis pathways were quantified by quantitative reverse transcriptase-polymerase chain reaction. Endothelial apoptosis was measured by Annexin V sta
SUBMITTER: Zavoriti A
PROVIDER: S-EPMC12678200 | biostudies-literature | 2025 Dec
REPOSITORIES: biostudies-literature