ArticlePloS one2012
Inflammation aggravates disease severity in Marfan syndrome patients.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Skeletal muscle alterations in Marfan syndrome: a systematic review.Journal of muscle research and cell motility · 2025Pooled it
- Circulating interleukin-6 (IL-6) levels are associated with aortic dimensions in genetic aortic conditions.PloS one · 2019Trial
- Downregulation ofMolecular therapy. Nucleic acids · 2026Article
- Perivascular inflammation in the progression of aortic aneurysms in Marfan syndrome.JCI insight · 2025Article
- Proteomic discoveries in hypermobile Ehlers-Danlos syndrome reveal insights into disease pathophysiology.ImmunoHorizons · 2025Article
- Sex- and age-dependent neurovascular abnormalities linked to neuroinflammation lead to exacerbated post-ischemic brain injury in Marfan syndrome mice.Redox biology · 2025Article
- Regnase-1 overexpression as a therapeutic approach of Marfan syndrome.Molecular therapy. Methods & clinical development · 2024Article
- Integrated DNA methylation analysis reveals a potential role for PTPRN2 in Marfan syndrome scoliosis.JOR spine · 2024Article
- Genetic Basis, New Diagnostic Approaches, and Updated Therapeutic Strategies of the Syndromic Aortic Diseases: Marfan, Loeys-Dietz, and Vascular Ehlers-Danlos Syndrome.International journal of environmental research and public health · 2023Review
- Association of MLL3 and TGF-β signaling gene polymorphisms with the susceptibility and prognostic outcomes of Stanford type B aortic dissection : MLL3 with TGF-β signal pathway association with Stanford type B AD.BMC cardiovascular disorders · 2023Article
- Aortic Wall Inflammation in the Pathogenesis, Diagnosis and Treatment of Aortic Aneurysms.Inflammation · 2022Review
- Treatment With Methotrexate Associated With Lipid Core Nanoparticles Prevents Aortic Dilation in a Murine Model of Marfan Syndrome.Frontiers in cardiovascular medicine · 2022Article
- Identification of crucial genes involved in pathogenesis of regional weakening of the aortic wall.Hereditas · 2021Article
- Amino Acid and Phospholipid Metabolism as an Indicator of Inflammation and Subtle Cardiomyopathy in Patients with Marfan Syndrome.Metabolites · 2021Article
- Potential predictors of severe cardiovascular involvement in Marfan syndrome: the emphasized role of genotype-phenotype correlations in improving risk stratification-a literature review.Orphanet journal of rare diseases · 2021Review
- An Overview of Investigational and Experimental Drug Treatment Strategies for Marfan Syndrome.Journal of experimental pharmacology · 2021Review
- The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms.International journal of molecular sciences · 2020Review
- Microarray analysis of long non-coding RNA expression profiles in Marfan syndrome.Experimental and therapeutic medicine · 2020Article
- Specific miRNA and Gene Deregulation Characterize the Increased Angiogenic Remodeling of Thoracic Aneurysmatic Aortopathy in Marfan Syndrome.International journal of molecular sciences · 2020Article
- Localized Antileptin Therapy Prevents Aortic Root Dilatation and Preserves Left Ventricular Systolic Function in a Murine Model of Marfan Syndrome.Journal of the American Heart Association · 2020Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMarfan syndrome (MFS) is a pleiotropic genetic disorder with major features in cardiovascular, ocular and skeletal systems, associated with large clinical variability. Numerous studies reveal an involvement of TGF-β signaling. However, the contribution of tissue inflammation is not addressed so far. METHODOLOGY/PRINCIPAL
findingsHere we showed that both TGF-β and inflammation are up-regulated in patients with MFS. We analyzed transcriptome-wide gene expression in 55 MFS patients using Affymetrix Human Exon 1.0 ST Array and levels of TGF-β and various cytokines in their plasma. Within our MFS population, increased plasma levels of TGF-β were found especially in MFS patients with aortic root dilatation (124 pg/ml), when compared to MFS patients with normal aorta (10 pg/ml; p = 8×10(-6), 95% CI: 70-159 pg/ml). Interestingly, our microarray data show that increased expression of inflammatory genes was associated with major clinical features within the MFS patients group; namely severity of the aortic root dilatation (HLA-DRB1 and HLA-DRB5 genes; r = 0.56 for both; False Discovery Rate(FDR) = 0%), ocular lens dislocation (RAET1L, CCL19 and HLA-DQB2; Fold Change (FC) = 1.8; 1.4; 1.5, FDR = 0%) and specific skeletal features (HLA-DRB1, HLA-DRB5, GZMK; FC = 8.8, 7.1, 1.3; FDR = 0%). Patients with progressive aortic disease had higher levels of Macrophage Colony Stimulating Factor (M-CSF) in blood. When comparing MFS aortic root vessel wall with non-MFS aortic root, increased numbers of CD4+ T-cells were found in the media (p = 0.02) and increased number of CD8+ T-cells (p = 0.003) in the adventitia of the MFS patients. CONCLUSION/SIGNIFICANCE: In conclusion, our results imply a modifying role of inflammation in MFS. Inflammation might be a novel therapeutic target in these patients.
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