Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: RNA-seq profiling of patients with heart failure

PROVIDER: PRJNA741605 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15002534.fastq.gz	Fastqsanger.gz
	SRR15002535.fastq.gz	Fastqsanger.gz
	SRR15002536.fastq.gz	Fastqsanger.gz
	SRR15002537.fastq.gz	Fastqsanger.gz
	SRR15002538.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 17

Similar Datasets

Project description:Genomic profiling of patients with heart failure

| PRJNA742541 | ENA

Project description:RNA-seq of peripheral blood cells from heart failure patients

| PRJNA532278 | ENA

Homo sapiens

Project description:RNA-seq analysis of human heart failure

| PRJNA239241 | ENA

Transcriptomics analysis of skeletal muscle in humans with heart failure

Project description:Heart failure is a multisystem syndrome caused by structural and functional defects in multiple tissues. The study aims to identify differentially regulated genes in skeletal muscle of heart failure patients. Here, we obtained biopsies from the pectoralis major muscle and performed RNA sequencing to profile the gene expression patterns from six heart failure patients and three healthy controls.

2020-09-07 | E-MTAB-8531 | biostudies-arrayexpress

Transcriptional profiling of human white blood cells at the different stages of NYHA classification

Project description:Human white blood cells from healthy, heart failure risk patients, asymptomatic left ventricular dysfunction patients, chronic heart failure, acute heart failure patients Common reference experiment, 9 replicates per group.

2012-05-02 | E-GEOD-21125 | biostudies-arrayexpress

Circulating microRNAs are candidate markers of heart failure and differentiate between heart failure with reduced vs preserved left ventricular ejection fraction.

Project description:In this study, we compared the expression profiles of circulating miRNAs in blood samples from controls and patients with heart ailment. Subject with no past history of heart failure/disease are considered as controls. The patients were classified according to the percentage of left ventricular ejection fraction. Patients were grouped as heart failure with reduced (hfREF) and preserved (hfPEF) left ventricular ejection fraction. Employing miRNA microarray, we identified 'signature miRNAs' in peripheral blood samples that distinguished Heart failure from the non-heart failure controls, as well as those of hfREF and hfPEF groups.

2015-02-12 | GSE53437 | GEO

Heart failure patients' peripheral blood mononuclear cell gene expression profiles before mechanical circulatory support

Project description:This data represents whole transcriptome total RNA gene expression profiles of peripheral blood mononuclear cells collected from 29 advanced heart failure patients on the day before undergoing mechanical circulatory support surgery. Keywords = Advanced Heart Failure. Keywords = Mechanical Circulatory Support. Keywords = Biological Age. Keywords = PBMC. Keywords = Immune Response. Keywords = Peripheral Blood. Keywords =Organ Function. Keywords = Recovery. Organism: Homo sapiens. Type: Expression profiling by array. Platforms: Illumina HiSeq 2500.

2018-02-13 | GSE104423 | GEO

Transcriptional profiling of human white blood cells at the different stages of NYHA classification

Project description:Human white blood cells from healthy, heart failure risk patients, asymptomatic left ventricular dysfunction patients, chronic heart failure, acute heart failure patients

2012-05-03 | GSE21125 | GEO

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [ChIP-Seq]

Project description:Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in heart failure. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during the evolution of heart failure. BET inhibition suppresses cardiomyocyte hypertrophy in a cell-autonomous manner, confirmed by RNA interference in vitro. Following both pressure overload and neurohormonal stimulation, BET inhibition potently attenuates pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to heart failure pathogenesis. Specifically, BET bromodomain inhibition in mice abrogates pathology-associated pause release and transcriptional elongation, thereby preventing activation of cardiac transcriptional pathways relevant to the gene expression profile of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in heart failure. ChIP-Seq of mouse heart tissues from mice induced with heart failure and treated with JQ1 BET bromodomain inhibitor

2013-08-06 | E-GEOD-46668 | biostudies-arrayexpress

GNPS - Metabolomic Insights in Advanced Cardiomyopathy of Chronic Chagasic and Idiopathic Patients that Underwent Heart Transplant

Project description:Characterization of plasma metabolomic profile of 15 patients with advanced heart failure referred for heart transplantation (8 patients with chronic chagasic cardiomyopathy and 7 with idiopathic dilated cardiomyopathy) and 12 heart donor individuals using gas chromatography/quadrupole time-of-flight mass spectrometry.

2023-07-25 | MSV000092522 | GNPS

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data