Abstract

Venous thromboembolism (VTE) is the comorbidity of deep vein thrombosis (DVT) and pulmonary embolism (PE); it is an urgent public health problem. The primary cause of venous thrombosis is endothelial dysfunction caused by vascular injury and inflammation or overexpressed procoagulant factors. Previous studies have shown that vascular endothelial cell apoptosis is involved in venous thrombosis, causing vascular wall damage. The pro-inflammatory cytokine interleukin-17 (Il-17A) induces endothelial cell apoptosis and promotes thrombosis. However, it remains unclear whether other IL-17 family cytokines are involved in thrombus formation. Among the IL-17 family, IL-17B is less well-characterized. Several studies have reported that IL-17B could stimulate TNF-α, IL-1, and IL-6 expression in macrophages. Furthermore, IL-17B induced activation of the ERK1/2 pathway, upregulating Bcl-2 family anti-apoptotic proteins in breast tumors. However, it is unclear whether IL-17B is involved in thrombus formation by regulating endothelial apoptosis. Therefore, this study aimed to examine whether IL-17B could affect endothelial apoptosis by promoting thrombus formation.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.