ArticleMediators of inflammation2026
Macrophage-Driven Bidirectional Exacerbation in Psoriasis-Atherosclerosis Comorbidity: Insights From a Novel Mouse Model.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Macrophage-Driven Bidirectional Exacerbation in Psoriasis-Atherosclerosis Comorbidity: Insights From a Novel Mouse Model.Mediators of inflammation · 2026Article
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16 authors.
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Abstract
backgroundPsoriasis (PSO) and atherosclerosis (AS) are chronic inflammatory diseases that frequently coexist, with each condition exacerbating the other. However, the underlying mechanisms remain poorly understood, partly due to the lack of a suitable animal model that recapitulates this bidirectional comorbidity.
methodsPSO-AS mouse models were constructed by combining high-fat diet (HFD)-induced AS with imiquimod (IMQ)-triggered psoriatic inflammation in ApoE
resultsChronic PSO model more closely resembles real-world conditions than acute PSO model. Combining the IMQ application with a HFD, both the PSO-AS group and the PSO group developed obvious psoriatic skin lesion, but the PSO-AS group showed the highest epidermal thickness, PASI scores, and expression levels of psoriatic biomarkers (Interleukin-17A [IL-17A] and Interleukin-23 [IL-23]) and inflammatory factors (e.g., tumor necrosis factor alpha [TNF-α] and Interleukin-6 [IL-6]), implying that AS may exacerbate PSO. Similarly, the PSO-AS and AS groups both developed obvious plaque in the aorta, while the PSO-AS group has the largest plaque area, necrotic core (NC) area, lipid content with the least fibrous cap (FC) thickness, and collagen content, illustrating that PSO conspicuously aggravated AS progression and led to an unstable plaque shift. Statistical analysis also confirms that PSO and AS mutually exacerbate each other, forming a vicious cycle that may be strongly associated with IL-17. Proteomics and ML revealed marked M1 macrophage polarization in PSO-AS mice. Validation by Western blot and IF showed upregulated M1 markers (CD86) and downregulated M2 markers (CD163) in both skin lesions and aortic roots, indicating that M1-skewed macrophages fuel the vicious cycle. Besides, we explore that IFIT3 may serve as a promising biomarker for M1 macrophages in PSO-AS skin.
conclusionsThis novel PSO-AS mouse model faithfully recapitulates the bidirectional exacerbation seen clinically and uncovers M1 macrophage polarization as a key driver of this comorbidity. The model provides a robust platform for mechanistic and therapeutic studies of PSO-associated cardiovascular disease (CVD).
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