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Interferon Regulatory Factors as Potential Therapeutic Targets in Cardiovascular Disease: Focusing on Vascular Inflammation

Year: 2026

Type: article

Abstract: The interferon regulatory factor (IRF) family exerts dual regulatory roles in vascular inflammation. Pro-inflammatory IRF1/3/5/7 drive endothelial dysfunction, macrophage M1 polarization, vascular smooth muscle cell (VSMC) transdifferentiation, and adaptive immune amplification via nuclear factor-κB (NF-κB), NOD-like receptor pyrin domain-containing 3 (NLRP3), cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. Conversely, IRF4/8 mediate anti-inflammatory effects by promoting M2 polarization, reverse cholesterol transport, and dendritic cell regulation. In atherosclerosis, IRFs display spatiotemporal specificity: endothelial IRF3 in early stages, macrophage IRF1/5 in mid-stages, and smooth muscle IRF7/IRF8 in late stages, supporting phase-specific precision interventions-early IRF3 blockade, mid-stage modulation of IRF5/IRF4 balance, and late combined inhibition of IRF7/8 to stabilize plaques. IRFs also critically participate in hypertensive remodeling, acute coronary syndrome, heart failure, and aortic aneurysm through conserved innate and adaptive immune axes, highlighting their potential as cross-disease biomarkers and therapeutic targets. Major challenges include network redundancy and functional compensation, necessitating single-cell multi-omics and targeted delivery systems for spatiotemporally precise, individualized modulation.

Source: International Journal of Molecular Sciences

DOI: 10.3390/ijms27177647

Authors: Chenxi Bai, Weixu Liu, Yubo Wang, Huixia Zhu, Xing Fan

Institution: Nantong 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: $3,499