ArticleRedox biology2025
CD40-TRAF6 inhibition suppresses cardiovascular inflammation, oxidative stress and functional complications in a mouse model of arterial hypertension.
Article in Redox biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Abdominal aortic aneurysm progression: A review of preclinical and clinical data.Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Identification and validation of a prognostic risk-scoring model in drug-resistant ALL and evaluation of immune micro-environment.Annals of hematology · 2026Article
- B cells and B-cell receptor repertoire features in coronary heart disease: immunopathogenic roles, clinical relevance, and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- Ubiquitination regulation in coronary microcirculation dysfunction: focus on the endothelial cells.Frontiers in cardiovascular medicine · 2026Review
- TRAF6 promotes pulmonary hypertension by enhancing K63-linked ubiquitination and activation of STAT3.Frontiers in pharmacology · 2026Article
- How Advanced Is Nanomedicine for Atherosclerosis?International journal of nanomedicine · 2025Review
- Diagnostic Value and Regulatory Mechanism of miR-322-5p in Coronary Heart Disease.Journal of inflammation research · 2025Article
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Authors and funding
16 authors.
Funding
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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 treatment normalized endothelial dysfunction and reduced blood pressure in hypertensive wild type animals. Reactive oxygen species production was decreased by TRAF6 inhibition in blood, aorta, heart, kidney, and perivascular fat tissue. Additionally, FACS analysis revealed that TRAF6 inhibition prevents immune cell migration into the aortic vessel wall observed by reduced CD45
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