EGAS00001000049-sc-20111117 - samples
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ABSTRACT:
PROVIDER: EGAD00001000053 | EGA |
REPOSITORIES: EGA
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Project description:The present study aimed to gain insights into the pathological process of Calcific Aortic Valve Disease (CAVD) in CHIP carriers. To this end, we screened for CHIP, by DNA sequencing of blood samples, a cohort of 168 patients with calcified aortic stenosis who had undergone valve replacement via transcatheter aortic valve implantation (TAVI) or surgically.
2022-08-02 | E-MTAB-11352 | biostudies-arrayexpress
Project description:Aortic valve cell heterogeneity increases during Aortic Valve Stenosis (AVS) progression. We used single cell RNA sequencing (scRNA-seq) to characterize valve cell phenotype in AVS patients.
2024-12-01 | GSE273980 | GEO
Project description:Calcific Aortic Valve Disease (CAVD) is a common heart valve condition, often characterized by severe narrowing of the aortic valve. It lacks pharmaceutical treatments and typically requires aortic valve replacement surgery, imposing a significant burden on healthcare resources.This study reports the expression profile of circRNAs in the aortic valve tissues of CAVD patients and a normal control group (non-CAVD). We collected aortic valve tissue samples from three CAVD patients who underwent aortic valve replacement surgery due to severe aortic valve stenosis, as well as aortic valve samples from non-CAVD patients who either received heart transplant surgery (recipient heart) or had their aortic valve removed due to aortic dissection. Overall, our research reveals the significant role of circRNAs in the progression of CAVD. CircRNAs, a class of circular non-coding RNA molecules, are actively studied for their functions and regulatory mechanisms within cells. These findings contribute to a deeper understanding of the molecular mechanisms underlying CAVD, particularly the potential involvement of circRNAs in this disease.
2024-02-02 | GSE254393 | GEO
Project description:We compared 15 severely diseased aortic valve sample to 16 control aortic valve samples using microRNA microarrays (Affymetrix GeneChip miRNA 2.0). The diseased samples were taken from areas of severe disease of aortic valves removed at aortic valve replacement for severe aortic stenosis. Control samples were obtained from macroscopically normal post-mortem aortic valves. In addition, we compared areas of mild or moderate disease on valves from participants with severe aortic stenosis to the same participant's severely diseased sample in seven participants.
2017-04-27 | E-MTAB-2766 | biostudies-arrayexpress
Project description:<p><strong>BACKGROUND:</strong> 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.</p><p><strong>METHODS:</strong> 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.</p><p><strong>RESULTS:</strong> 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.</p><p><strong>CONCLUSIONS:</strong> 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.</p>
2020-02-03 | MTBLS1267 | MetaboLights
Project description:Calcified aortic valve leaflets (CAVs) were explanted from patients with severe aortic valve stenosis undergoing aortic valve replacement at the Department of Cardiovascular Surgery, Union Hospital, affiliated to Tongji Medical College. Control non-calcified aortic valves with normal echocardiographic analyses were obtained during heart transplant procedures. RNA was extracted from valve leaflets and gene expression evaluated using the Arraystar Human mRNA Array. This study aimed to perform the expression analysis of mRNA on human aortic valves.
2020-07-26 | GSE155119 | GEO
Project description:We aimed to disclose specific LV myocardial protein signatures possibly contributing to differential disease progression after aortic valve surgery in patients with chronic aortic stenosis and patients with chronic aortic regurgitation.
2023-05-10 | PXD039662 | Pride
Project description:Although calcific aortic valve stenosis (CAVS) is the most prevalent valvular heart disease, the molecular mechanisms underlying aortic valve calcification remain unknown. Here, we found a significant elevation in stanniocalcin-1 (STC1) expression in the valve interstitial cells (VICs) of calcific aortic valves by combined analysis of our comprehensive gene expression data and microarray datasets reported previously. Immunohistochemical staining showed that STC1 was located around the calcific area in the aortic valves of patients with CAVS. In vitro experiments using inhibitors and siRNA targeting osteoblast differentiation signaling revealed that activation of the Akt/STC1 axis was essential for runt-related transcription factor 2 (RUNX2) induction in the VICs. RNA sequencing and bioinformatics analysis of STC1-knocked down VICs in osteoblast differentiation medium resulted in silencing of the induction of osteoarthritis signaling-related genes, including RUNX2 and COL10A1. STC1 depletion in the murine CAVS model improved aortic valve dysfunction with high peak velocity and valve thickening and suppressed the appearance of osteochondrocytes. STC1-deficient mice also exhibited complete calcification abolishment, although partial valve thickening by aortic valve injury was observed. Our findings suggest that STC1 may be a critical factor in determining valve calcification and a novel target for preventing the transition to severe CAVS with calcification. We analyzed the gene expression profiles of the valve interstitial cells (VICs) isolated from noncalcific and calcific areas in calcific aortic valve stenosis (CAVS) donors using a gene microarray.
2023-12-31 | GSE226781 | GEO
Project description:Calcific aortic valve disease (CAVD) is an slowly progressive calcification of heart valve which leads to aortic stenosis. The only existing treatment of CAVD is surgical replacment of calcified valve - development of anti-CAVD treatment is urgent task. For better understanding of molecular mechanisms of CAVD progression we performed proteomics analysis of osteogenic differentiation of human valve interstitial cells isolated from healthy humans or patients with CAVD.
2022-10-21 | PXD032212 | Pride
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