CD40-TRAF6 inhibition suppresses cardiovascular inflammation, oxidative stress and functional complications in a mouse model of arterial hypertension.

ABSTRACT: Cardiovascular disease is the leading cause of disease burden and death worldwide and is fueled by vascular inflammation. CD40L-CD40-TRAF signaling is involved in the progression of atherosclerosis and drives the development of coronary heart disease (CHD). The present study investigates whether the CD40L-CD40-TRAF6 signaling pathway with focus on immune cells and adipocytes could be a therapeutic target in arterial hypertension. Arterial hypertension was induced in WT (C57BL6/J) and cell-specific CD40(L) knockout mice (AdipoqCre x CD40 fl/fl, CD4Cre x CD40 fl/fl, CD19Cre x CD40 fl/fl, and GP1baCre x CD40L fl/fl) via angiotensin (AT-II) infusion (1 mg/kg/d) for seven days. Hypertensive WT mice were also treated with a CD40-TRAF6 inhibitor (2.5 mg/kg/d, for 7d). The TRAF6 inhibitor treatmen

SUBMITTER: Strohm L 

PROVIDER: S-EPMC11840497 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature