ArticleResearch (Washington, D.C.)2025
Elevated Dickkopf 3 Promotes Abdominal Aortic Aneurysm Formation via Modulated Phenotype Switch of Vascular Smooth Muscle Cells.
Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Targeting RUNX3 alleviates abdominal aortic aneurysm by ameliorating oxidative stress via mitophagy.Journal of thrombosis and thrombolysis · 2026Article
- FAM177A1 disrupts SIRT3-SOD2 signaling to drive mitochondrial dysfunction-mediated VSMC phenotypic switching in vascular remodeling.International journal of biological sciences · 2026Article
Corrections and comments
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Authors and funding
16 authors.
Funding
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Abstract
Abdominal aortic aneurysm (AAA) is a potentially fatal vascular disease with no effective therapeutic intervention. Vascular smooth muscle cell (VSMC) phenotypic switching and elevated matrix metalloproteinase (MMP) levels are key pathogeneses of AAA, although the underlying regulatory mechanisms remain to be fully elucidated. In our study, single-cell RNA-sequencing data analysis demonstrated a substantial elevation in modulated VSMCs in patients with aortic aneurysm, accompanied by Dickkopf 3 (DKK3) up-regulation. Both systemic DKK3 knockout and VSMC-specific DKK3 knockdown led to a marked decrease in both the incidence and mortality of AAA in mice. Reintroduction of DKK3 in
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