ArticleScientific reports2026
The vasoprotective role of Myeloid-derived suppressor cells in pathogenesis of aortic dissection.
Article in Scientific reports, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Myeloid-Derived Suppressor Cells (MDSCs) in Cardiovascular Risk of Obesity-Associated Diabetes.International journal of molecular sciences · 2026Review
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5 authors.
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Abstract
In patients with cardiovascular diseases, myeloid-derived suppressor cells (MDSCs) play important regulatory roles in the inflammatory response and have protective effects. Aortic dissection (AD) is a vascular disease with complex pathogenesis, and inflammation and immune cells are considered key factors in the occurrence and development of AD. The role of MDSCs in patients with AD remains unclear. The proportions of MDSCs in the peripheral blood and spleens of mice were determined by flow cytometry. The effects of MDSCs on AD model mice were observed upon depletion of MDSCs with 5-fluorouracil. Changes in the vascular walls were observed by pathological HE staining. Inflammatory factors were detected by enzyme-linked immunosorbent assays. The proportion of monocytic myeloid-derived suppressor cells (M-MDSCs) in the spleens of AD model mice increased. The number of MDSCs in peripheral blood did not change, suggesting that MDSCs exert immune-modulating effects through aggregation and activation in immune organs. The increase in the number of M-MDSCs in the spleen was time dependent, and the increase was most significant during the later period of modeling. Microscopic observation revealed that the degree of aortic wall damage in AD model mice significantly increased after MDSCs were eliminated, including the expansion of intima tears, the aggravation of media dissociation, and the increase in inflammatory cell infiltration; this was further confirmed by pathological examination. After the MDSCs were depleted, proinflammatory factor IL-6 levels increased, anti-inflammatory factor IL-10 levels decreased, and aortic wall damage significantly worsened. MDSCs may be involved in the pathogenesis of AD through the regulation of inflammatory factors. Our results reveal that vasoprotective role of MDSCs in the development of AD. Depleting MDSCs exacerbates disease pathology, suggesting that enhancing or modulating the function of MDSCs may be a promising preventive and therapeutic strategy for patients with AD.
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