<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Metabolomics</omics_type><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>Ian Donaldson</submitter><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>RNA-seq of coding RNA</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16712</full_dataset_link><description>We aim to study the gene alteration in diabetic failing heart and decipher the molecular mechanisms underlying diabetes-associated heart failure. Diabetic patients are more vulnerable to cardiac dysfunction. The pathogenesis of diabetes-associated heart failure is multiple, including cardiac pathological remodeling, intracellular metabolic disorders, cardiac inflammation, etc. To determine which signaling pathways causes the myocardial alterations, we plan to identify the individual gene function during the pathogenesis using an unbiased large-scale screening. Firstly, gene expression should be assessed. RNA-seq is used to detect gene changes, afterwards, the potential candidates involved in the molecular basis induing diabetic heart failure will be validated by other assessment and function study will be performed to explore their role in the onset and progression of heart failure in diabetes. Samples are healthy subject versus those with diabetes with cardiovascular disease (CVD) and heart failure (HF)</description><repository>biostudies-arrayexpress</repository><sample_protocol>Sequencing - Samples were sequenced on an Illumina NovaSeq 6000 as per manufacturers instructions.</sample_protocol><sample_protocol>Nucleic Acid Extraction - Total RNA from the heart tissue was extracted using TRIzol and treated with DNAse (ThermoFisher Scientific, AM1906) to eliminate genomic DNA contamination. The quality and integrity of total RNA samples were checked using a 2100 Bioanalyzer (Agilent Technologies).  Samples were enriched for 3'-polyadenylated transcripts.</sample_protocol><sample_protocol>Sample Collection - The hearts were collected and snap-frozen in liquid nitrogen by BioIVT under proper licence and consent agreement; then imported under proper MTA and stored in -80 degree freezer with HTA licence before usage.</sample_protocol><sample_protocol>Library Construction - Library preparation of samples was performed using the Illumina TruSeq Stranded mRNA Sample Preparation Kits (Illumina).</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>Ian Donaldson</pubmed_authors><pubmed_authors>Wei Liu</pubmed_authors></additional><is_claimable>false</is_claimable><name>RNAseq of human heart tissue from healthy and failing hearts</name><description>We aim to study the gene alteration in diabetic failing heart and decipher the molecular mechanisms underlying diabetes-associated heart failure. Diabetic patients are more vulnerable to cardiac dysfunction. The pathogenesis of diabetes-associated heart failure is multiple, including cardiac pathological remodeling, intracellular metabolic disorders, cardiac inflammation, etc. To determine which signaling pathways causes the myocardial alterations, we plan to identify the individual gene function during the pathogenesis using an unbiased large-scale screening. Firstly, gene expression should be assessed. RNA-seq is used to detect gene changes, afterwards, the potential candidates involved in the molecular basis induing diabetic heart failure will be validated by other assessment and function study will be performed to explore their role in the onset and progression of heart failure in diabetes. Samples are healthy subject versus those with diabetes with cardiovascular disease (CVD) and heart failure (HF)</description><dates><release>2026-08-14T00:00:00Z</release><modification>2026-08-14T09:19:13.921Z</modification><creation>2026-03-03T11:37:33.541Z</creation></dates><accession>E-MTAB-16712</accession><cross_references><ENA>ERP189826</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0003738</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>