Ontology highlight
ABSTRACT:
PROVIDER: PRJNA943176 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Molecular analysis of the effect left ventricular assist device (LVAD) support has on congestive heart failure patients. Keywords = Congestive heart failure, left ventricular assist device, eNOS, gene, dimethylarginine dimethylaminohydrolase Keywords: other
2003-09-01 | GSE430 | GEO
Project description:Molecular analysis of the effect left ventricular assist device (LVAD) support has on congestive heart failure patients.
2007-12-13 | E-GEOD-430 | biostudies-arrayexpress
Project description:Effect of left ventricular assist device support on congestive heart failure patients
| PRJNA85003 | ENA
Project description:19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as ischemic (I) showing evidence of coronary artery disease, non-ischemic (N) no evidence of coronary artery disease or acute Myocardial infarction (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip.
2007-10-02 | E-GEOD-974 | biostudies-arrayexpress
Project description:19 paired human left ventricular apex samples were harvested at the time of implant of a left ventricular assist device (PRE) and at the time of explant (POST). The cohort included patients that were clinically classified as "ischemic" (I) showing evidence of coronary artery disease, "non-ischemic" (N) no evidence of coronary artery disease or "acute Myocardial infarction" (IM) myocardial infarction within 10 days of the implant. Tissue was processed and hybridized to the Affymetrix HG-U133A chip. Keywords: other
2004-01-18 | GSE974 | GEO
Project description:Exploratory Study on the Mechanism of Left Ventricular Function Recovery After Left Ventricular Assist Device Implantation in Pediatric Dilated Cardiomyopathy
| PRJNA1202226 | ENA
Project description:Heart failure is associated with high morbidity and mortality and its incidence increases worldwide. MicroRNAs (miRNAs) are potential markers and targets for diagnostic and therapeutic applications, respectively. We determined myocardial and circulating miRNA abundance and its changes in patients with stable and end-stage heart failure before and at different time points after mechanical unloading by a left ventricular assist device (LVAD) by small-RNA-sequencing. MiRNA changes in failing heart tissues partially resembled that of fetal myocardium. Consistent with prototypical miRNA–target-mRNA interactions, target mRNA levels were negatively correlated to changes in abundance for highly expressed miRNAs in heart failure and fetal hearts. The circulating small RNA profile was dominated by miRNAs, and fragments of tRNAs and small cytoplasmic RNAs. Heart- and muscle-specific circulating miRNAs (myomirs) increased up to 140-fold in advanced heart failure, which coincided with a similar increase in cardiac troponin I protein, the established marker for heart injury. These extracellular changes nearly completely reversed 3 months following initiation of LVAD support. In stable heart failure, circulating miRNAs showed less than 5-fold differences compared to normal, and myomir and cardiac troponin I levels were only captured near the detection limit. These findings provide the underpinning for miRNA-based therapies and emphasize the usefulness of circulating miRNAs as biomarkers for heart injury performing similar to established diagnostic protein biomarkers. Total RNA isolated from human left ventricular myocardium of failing hearts due to dilated or ischemic cardiomyopathy before and after mechanical unloading by a left ventricular assist device (LVAD), and fetal myocardium compared to non-failing postnatal myocardium.
2014-07-02 | E-GEOD-52601 | biostudies-arrayexpress
Project description:Heart failure is associated with high morbidity and mortality and its incidence increases worldwide. MicroRNAs (miRNAs) are potential markers and targets for diagnostic and therapeutic applications, respectively. We determined myocardial and circulating miRNA abundance and its changes in patients with stable and end-stage heart failure before and at different time points after mechanical unloading by a left ventricular assist device (LVAD) by small-RNA-sequencing. MiRNA changes in failing heart tissues partially resembled that of fetal myocardium. Consistent with prototypical miRNAM-bM-^@M-^Starget-mRNA interactions, target mRNA levels were negatively correlated to changes in abundance for highly expressed miRNAs in heart failure and fetal hearts. The circulating small RNA profile was dominated by miRNAs, and fragments of tRNAs and small cytoplasmic RNAs. Heart- and muscle-specific circulating miRNAs (myomirs) increased up to 140-fold in advanced heart failure, which coincided with a similar increase in cardiac troponin I protein, the established marker for heart injury. These extracellular changes nearly completely reversed 3 months following initiation of LVAD support. In stable heart failure, circulating miRNAs showed less than 5-fold differences compared to normal, and myomir and cardiac troponin I levels were only captured near the detection limit. These findings provide the underpinning for miRNA-based therapies and emphasize the usefulness of circulating miRNAs as biomarkers for heart injury performing similar to established diagnostic protein biomarkers. Total RNA isolated from human left ventricular myocardium of failing hearts due to dilated or ischemic cardiomyopathy before and after mechanical unloading by a left ventricular assist device, and fetal myocardium compared to non-failing postnatal myocardium was subjected to multiplexed small RNA-sequencing on the Illumina platform. mRNA gene expression data using Illumina HumanHT-12v4 beadarrays for a subset of the myocardial samples is available (GSE52601).
2014-07-02 | E-GEOD-53080 | biostudies-arrayexpress
Project description:Cardiac reverse remodeling occurs in a small subset of heart failure patients treated with guideline-directed therapies. This phenomenon, which is defined by reduced ventricular dilatation and improved systolic function, is most common in patients receiving left ventricular assist device (LVAD) therapy. Identifying therapeutic targets for initiating reverse remodeling is an area of great clinical interest, as these 40 patients experience improved outcomes and quality of life. Targets may be discovered among the unique molecular changes associated with partial myocardial functional recovery induced by LVAD; however, the mechanisms underlying this favorable response are incompletely understood. To identify molecular signatures of recovery, we studied paired pre- and post-LVAD myocardial samples from heart failure patients who received LVAD as a bridge-to-transplant (10 responders, 9 non-responders) and non-failing controls. We performed bulk RNA-sequencing, tandem-mass-tag (TMT) quantitative proteomics, and TMT quantitative phospho-proteomics with follow-up mechanistic and functional 50 investigations in primary rodent cardiomyocytes and human engineered heart tissues (EHTs).
2026-01-12 | PXD068672 | Pride
Project description:Cardiac reverse remodeling occurs in a small subset of heart failure patients treated with guideline-directed therapies. This phenomenon, which is defined by reduced ventricular dilatation and improved systolic function, is most common in patients receiving left ventricular assist device (LVAD) therapy. Identifying therapeutic targets for initiating reverse remodeling is an area of great clinical interest, as these 40 patients experience improved outcomes and quality of life. Targets may be discovered among the unique molecular changes associated with partial myocardial functional recovery induced by LVAD; however, the mechanisms underlying this favorable response are incompletely understood. To identify molecular signatures of recovery, we studied paired pre- and post-LVAD myocardial samples from heart failure patients who received LVAD as a bridge-to-transplant (10 responders, 9 non-responders) and non-failing controls. We performed bulk RNA-sequencing, tandem-mass-tag (TMT) quantitative proteomics, and TMT quantitative phospho-proteomics with follow-up mechanistic and functional 50 investigations in primary rodent cardiomyocytes and human engineered heart tissues (EHTs).
2026-01-12 | PXD068397 | Pride