ArticleInternational journal of medical sciences2024
RBM15 activates glycolysis in M1-type macrophages to promote the progression of aortic aneurysm and dissection.
Article in International journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Molecular mechanisms of programmed cell death in aortic dissection and advances in clinical translation.Molecular biology reports · 2026Review
- RBM15 in diseases: Molecular mechanisms and clinical opportunities from RNA mGenes & diseases · 2026Review
- Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026Review
- mFrontiers in cell and developmental biology · 2026Review
- The role of macrophages in aortic physiology and pathophysiology.Frontiers in immunology · 2026Review
- Total saponins ofJournal of ginseng research · 2025Article
- Lactylation associated biomarkers and immune infiltration in aortic dissection.Scientific reports · 2025Article
- Myeloid Cells in Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2025Review
- RNA Binding Motif Protein 15 (RBM15): Structure, Function and Its Research Progress in Tumors.International journal of general medicine · 2025Review
- Development and Validation of the Systemic Inflammatory Response Index-Based Nomogram for Predicting Short-Term Adverse Events in Patients With Acute Uncomplicated Type B Aortic Intramural Hematoma.Journal of inflammation research · 2025Article
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4 authors.
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Abstract
Aortic aneurysm and dissection (AD) represent a critical cardiovascular emergency with an alarmingly high mortality rate. Recent research has spotlighted the overexpression of genes associated with the m6A modification in AD patients, linking them to the presence of inflammatory M1-type macrophages. Moreover, glycolysis is widely recognized as a key feature of inflammatory M1-type macrophages, but biomarkers linking glycolysis and macrophage function to promote disease progression in AD have not been reported. We conducted an analysis of aortic immune cell infiltration, macrophages, and m6A-related biomarkers in AD patients using bioinformatics techniques. Subsequently, we employed a combination of RT-PCR, WB, and immunofluorescence assays to elucidate the alterations in the expression of M1- and M2-type macrophages, as well as markers of glycolysis, following the overexpression of key biomarkers. These findings were further validated
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