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Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

ABSTRACT: Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

PROVIDER: PRJNA427313 | ENA |

REPOSITORIES: ENA

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Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

Project description:This study demonstrates that arthritis and heart valve stenosis comorbidity, the most common condition among RA and SpA patients, share common mesenchymal requirements converging in the pathogenic activation of resident mesenchymal origin fibroblasts in the TnfARE mouse model. TNFR2 signaling, in this context, orchestrates the molecular mechanisms underlying arthritis and heart valve stenosis manifestation by regulating fibroblasts pathogenic activation status, cell proliferation and pro-inflammatory milieu. Finally this work highlights the complexity of TNFR2 functions since mesenchymal signaling is detrimental, whereas systemic TNFR2 provides protective signals that contain both pathologies

2018-04-23 | GSE108451 | GEO

Mechanisms of Fibrotic Aortic Valve Stenosis

Project description:To examine molecular mechanisms of aortic valve stenosis in mice with hypertension and hypercholesterolemia, RNA-Seq was used during the developmental phase of stenosis to identify new gene targets.

2016-03-07 | GSE71534 | GEO

Metabolomics Characterization of Human Calcific Aortic Valve Stenosis

Project description:BACKGROUND: Calcific aortic valve stenosis (CAVS) is the most prevalent valvular heart disease in developed countries with significant morbidity and mortality. Given the poor understanding of the pathophysiological processes leading to CAVS, we utilized a joint non-targeted metabolomics and targeted lipidomics approach to better characterize the metabolic perturbations involved in its development and progression.METHODS: We collected human aortic valve tissue from 106 patients undergoing aortic valve replacement surgery. Our cohort represented aortic valvular hemodynamics from mild to severe aortic stenosis with varying degrees of valvular calcification.RESULTS: Seventy-two significantly differential (p<0.01) metabolites across different stages of CAVS severity were filtered and identified from the tissue metabolome. Each stage of valvular stenosis was characterized by a distinct metabolic signature. The top three perturbed metabolic pathways in the setting of CAVS involved glycerophospholipid metabolism, linoleic acid metabolism and primary bile acid biosynthesis. The lysophosphatidic acid species (LysoPA) exhibited significant (p<0.05) association with CAVS severity and were also found to select patients with accelerated rate of CAVS progression. Two LysoPA species namely, 18:2 LysoPA and 20:4 LysoPA, exhibited potential to serve as biomarkers of CAVS severity.CONCLUSIONS: The present study reports the largest and most comprehensive metabolomics analysis of human aortic valve stenosis that highlights the dysregulated LysoPA pathway involved in the pathogenesis of CAVS.

2020-02-03 | MTBLS1267 | MetaboLights

GWAS on Calcific Aortic Valve Stenosis

Project description:GWAS on Calcific Aortic Valve Stenosis

| PRJNA420788 | ENA

GWAS on Calcific Aortic Valve Stenosis

Project description:GWAS on Calcific Aortic Valve Stenosis

| PRJNA420787 | ENA

Aortic Valve Tissue: Stenosis vs. Sclerosis

Project description:Aortic Valve Tissue: Stenosis vs. Sclerosis

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Transcription profiling of human heart characterizing the progression of heart failure in patients with aortic valve stenosis

Project description:Myocardial left ventricular biopsies from male patients (n=6) with isolated aortic stenosis and pronounced left ventricular hypertrophy undergoing aortic valve replacement were harvested either from hearts with normal ejection fraction (EF,>50%) or with low EF (<30%). Biopsies were further obtained from non-hypertrophied hearts with normal EF (>60%) from coronary artery disease patients undergoing coronary artery bypass graft surgery (n=3). Total RNA isolated from biopsies was analyzed using Affymetrix HG-U133A and U133B GeneChip sets.

2010-12-15 | E-MEXP-2296 | biostudies-arrayexpress

Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.

Project description: Not available

| S-EPMC5928856 | biostudies-literature

Myocardial proteome profiling reveals disease- and sex-specific alterations in patients with aortic valve stenosis and mitral valve regurgitation

Project description:Heart valve diseases, such as aortic valve stenosis (AS) and mitral valve regurgitation (MR), are leading causes of heart failure. However, myocardial proteome studies in AS and MR are extremely rare. We profiled the proteome of 75 human left ventricular myocardial biopsies (AS=41, MR=17, controls=17) and detected disease- and sex-specific protein expression alterations. Patients with AS, for example, showed higher abundance of fibrosis-related proteins and lower abundance of proteins related to energy metabolism and protein synthesis capacity with prominent sex differences. This might explain the higher amount of myocardial mass and fibrosis and lower systolic cardiac function especially observed in male AS in our cohort and might help to find specific proteins as treatment targets. Our work provides detailed insight into myocardial protein alterations in AS and MR and expands, in combination with clinical parameters, the understanding of cardiac remodeling in female and male patients, aiming to improve disease- and sex-specific therapy.

2022-12-13 | PXD023800 | Pride

Expression data of human aortic valve cusps

Project description:Calcific aortic valve disease is the most common form of valvular heart disease in the Western World. Milder degrees of aortic valve calcification is called aortic sclerosis and severe calcification with impaired leaflet motion is called aortic stenosis. We used microarrays to detail the global programme of gene expression underlying cdevelopment of calcified aortic valve disease in humans.

2015-10-01 | GSE51472 | GEO

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