Work

IRF6 induces endothelial dysfunction through the transcriptional activation of NDRG1 and aggravates low shear stress-mediated atherosclerosis

Year: 2026

Type: article

Abstract: mice. After four weeks of feeding, AS mice exhibited higher IRF6 expression and more severe lesions than sham mice. IRF6 suppression alleviated ED, inflammatory response, and oxidative stress in LSS-induced AS mice. In LSS-treated human aortic endothelial cells (HAECs), IRF6 was also highly expressed. Inhibition of IRF6 reduced the expression of pro-inflammatory adhesion molecules and the adhesion of THP-1 cells to HAECs. Mechanistically, IRF6 transcriptionally upregulated NDRG1. NDRG1 upregulation reversed the beneficial effect of IRF6 knockdown. Overall, IRF6 induces ED through the transcriptional activation of NDRG1, aggravating LSS-mediated AS progression.

Source: iScience

DOI: 10.1016/j.isci.2026.115127

Authors: Yong Chen, Yanchao Zhang, Shen Rui, Bo Dong, Xiangshan Xu, Yuanzhe Jin

Institutions: Fourth Affiliated Hospital of China Medical University, China Medical University

Language: English

Topic: Atherosclerosis and Cardiovascular Diseases

Subfield: Immunology

Field: Immunology and Microbiology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $3,240