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ISG15 links type I interferon pathway to cardiovascular risk in systemic lupus erythematosus
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DOI：10.1007/s10238-026-02275-4.png)
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Abstract
En 中文
Patients with systemic lupus erythematosus (SLE) have significantly increased cardiovascular risk, and atherosclerosis (AS) is a major cause of long-term mortality. However, whether SLE-specific immune dysregulation drives accelerated AS remains unclear. This study explored the role of interferon-stimulated gene 15 (ISG15) in SLE-associated AS. We first characterized the disease manifestations, then identified disease characteristics at the proteomic and transcriptomic levels via multi-omics analysis of a pristane-induced SLE-ApoE−/− mouse model and integrated analysis of SLE and AS datasets. We found ISG15 was uniquely elevated across atherosclerotic plaque types and correlated with cardiovascular events, with robust interferon-alpha response activation in SLE mice. Further, ISG15 colocalized with CD68⁺ macrophages in plaques, and extended analysis showed it was highly expressed in peripheral blood monocytes of SLE patients. Clinically, ISG15⁺ monocyte proportion was significantly higher in SLE patients with AS, outperforming conventional cardiovascular risk scores and serving as an independent predictor. In conclusion, ISG15 is a critical effector linking SLE immune dysregulation to accelerated AS, and ISG15⁺ monocyte proportion is a promising biomarker for cardiovascular risk stratification in SLE patients.
Keywords:
Systemic lupus erythematosus
Atherosclerosis
ISG15
Type I interferon
Biomarker
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