ArticleAnnals of medicine and surgery (2012)2025
Metabolomics analysis of acute lung injury induced by aortic dissection in mice.
Article in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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6 authors.
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Abstract
Thoracic aortic aneurysm/dissection (TAA/D) is a complicated vascular disorder with galloping development and high mortality. Phenotype switching plays an important role in the pathological process of TAA/D. Previous studies indicated the potential correlation between the expression level of lncRNA RP11-465L10.10 and MMP9 involved in the development of TAA/D. Here, our results showed that RP11-465L10.10 and MMP9 were highly increased in TAD patient tissues, which was consistent in Ang II-induced vascular smooth muscle cell (VSMC) phenotype switching. However, the effects and underlying mechanism of RP11-465L10.10 on VSMC phenotypic switching remain uncertain. Therefore, the expression of SM22α, cell proliferation, and migration were investigated when ectopically expressed RP11-465L10.10 in VSMCs. The results showed that RP11-465L10.10 overexpression decreased SM22α expression and facilitated VSMC proliferation, migration, and MMP9 expression. Furthermore, the NF-κB signaling pathway was enriched in transcriptome data analysis, indicating that NF-κB signaling may be involved in RP11-465L10.10-induced VSMC phenotype switching and MMP9 expression. In conclusion, this study demonstrated that RP11-465L10.10 induces VSMC phenotype switching and MMP9 expression via the NF-κB signaling pathway, suggesting that RP11-465L10.10 might be a potential therapeutic target for TAA/D treatment.
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