ArticleArteriosclerosis, thrombosis, and vascular biology2019
Glycoproteomic Analysis of the Aortic Extracellular Matrix in Marfan Patients.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Single-Cell Proteomics Uncovers Cell-Specific Proteins in Vascular Health and Marfan Syndrome Disease-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Aortic Stenosis Hyalectan Remodeling Revealed by Proteomics and Glycoproteomics.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Excessive glycosylation drives thoracic aortic aneurysm formation through integrated stress response.European heart journal · 2025Article
- Sex- and region-specific differences in microstructural remodeling and passive biomechanics of the aorta correlate with aneurysm propensity in a mouse model of severe Marfan syndrome.Acta biomaterialia · 2025Article
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- Comparative Analysis of Perivascular Adipose Tissue Attenuation on Chest Computed Tomography Angiography in Patients with Marfan Syndrome: A Case-Control Study.Diagnostics (Basel, Switzerland) · 2025Article
- Sensitivity to Aortic Rupture in Hereditary Aortic Diseases.Thrombosis and haemostasis · 2025Article
- Microfibril-associated glycoprotein 4 forms octamers that mediate interactions with elastogenic proteins and cells.Nature communications · 2024Article
- Non-Coding RNA-Targeted Therapy: A State-of-the-Art Review.International journal of molecular sciences · 2024Review
- Versican accumulation drives Nos2 induction and aortic disease in Marfan syndrome via Akt activation.EMBO molecular medicine · 2024Article
- Human stem cell models for Marfan syndrome: aFrontiers in cell and developmental biology · 2024Review
- Identification of co-diagnostic effect genes for aortic dissection and metabolic syndrome by multiple machine learning algorithms.Scientific reports · 2023Article
- Multi-omics in thoracic aortic aneurysm: the complex road to the simplification.Cell & bioscience · 2023Review
- Article
- FN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Review
- MicroRNAs as therapeutic targets in cardiovascular disease.The Journal of clinical investigation · 2022Review
- Biomarkers in EndoVascular Aneurysm Repair (EVAR) and Abdominal Aortic Aneurysm: Pathophysiology and Clinical Implications.Diagnostics (Basel, Switzerland) · 2022Review
- Vascular Stem/Progenitor Cells in Vessel Injury and Repair.Frontiers in cardiovascular medicine · 2022Review
- Applying multi-omics techniques to the discovery of biomarkers for acute aortic dissection.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
23 authors at 10 institutions in 3 countries.
Funding
Abstract
objectiveMarfan syndrome (MFS) is caused by mutations in FBN1 (fibrillin-1), an extracellular matrix (ECM) component, which is modified post-translationally by glycosylation. This study aimed to characterize the glycoproteome of the aortic ECM from patients with MFS and relate it to aortopathy. Approach and Results: ECM extracts of aneurysmal ascending aortic tissue from patients with and without MFS were enriched for glycopeptides. Direct N-glycopeptide analysis by mass spectrometry identified 141 glycoforms from 47 glycosites within 35 glycoproteins in the human aortic ECM. Notably, MFAP4 (microfibril-associated glycoprotein 4) showed increased and more diverse N-glycosylation in patients with MFS compared with control patients. MFAP4 mRNA levels were markedly higher in MFS aortic tissue. MFAP4 protein levels were also increased at the predilection (convexity) site for ascending aorta aneurysm in bicuspid aortic valve patients, preceding aortic dilatation. In human aortic smooth muscle cells, MFAP4 mRNA expression was induced by TGF (transforming growth factor)-β1 whereas siRNA knockdown of MFAP4 decreased FBN1 but increased elastin expression. These ECM changes were accompanied by differential gene expression and protein abundance of proteases from ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family and their proteoglycan substrates, respectively. Finally, high plasma MFAP4 concentrations in patients with MFS were associated with a lower thoracic descending aorta distensibility and greater incidence of type B aortic dissection during 68 months follow-up.
conclusionsOur glycoproteomics analysis revealed that MFAP4 glycosylation is enhanced, as well as its expression during the advanced, aneurysmal stages of MFS compared with control aneurysms from patients without MFS.
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