Similar Datasets
Project description:Heart failure (HF) impacts 2-3% of adults in the West, with prevalence rising with age. This condition, leading to high mortality and morbidity, increasingly involves HF with preserved left ventricular (LV) ejection fraction (HFpEF) in the aging population, having a similar stable prognosis as HF with reduced LVEF (HFrEF). However, HFpEF lacks many evidence-based therapies, partly due to its distinct pathophysiology compared to HFrEF. Molecularly, heart failure shows distinct gene expression changes, indicative of varying diseases. Prior research, including our early report from the CABG-PREFERS study, shows gene expression differences in HFpEF and normal hearts, although studies are limited. Both HFpEF and HFrEF patients exhibit altered LV myocardial structure and function, often affecting the right ventricle (RV) secondarily. In the CABG-PREFERS sub-study, part of the PREFERS programme, we classified patients by LVEF, structural abnormalities, diastolic dysfunction, and NT-proBNP levels into HFpEF physiology, HFrEF physiology, and normal LV function groups. Our hypothesis suggests gene expression and transcriptomic variations between LV and RV, and between HFpEF, HFrEF, and normal LV function, providing insights into different HF phenotypes and guiding future therapies.
2024-02-28 | E-MTAB-13553 | biostudies-arrayexpress
Project description:Metabolomic and Transcriptomic Signatures of Chemnogenetic Heart Failure
| PRJNA802683 | ENA
Project description:We analyzed time dependent global proteomic adaptations during heart failure (HF) progression in a mouse model, suffering from left ventricular pressure overload due to transverse aortic constriction (TAC), to gain deeper insights in the disease development and identify new biomarker candidates. The hearts from TAC and sham mice were examined by cardiac MRI on either day 4, 14, 21, 28, 42, and 56 after surgery (n=6 group/time point). At each time point, proteomes of the left (LV) and right ventricles (RV) of TAC and sham mice were analyzed by mass spectrometry (MS).
2018-07-16 | PXD007171 | Pride
Project description:Analysis of changes of gene expression profiles in the left ventricle (LV) during the progression of heart failure (HF) in the canine tachypacing induced HF model. Gene expression profiling was performed on samples collected at different time points representing various stages of LV dysfunction, i.e. tachypaced for 3 days (Day-3), 1 week (Week-1), 2 weeks (Week-2), 3-4 weeks (End stage), and unpaced controls (Day-0). Results provide insights into molecular mechanisms of heart failure progression. Keywords: time course This work aims to study changes of gene expression profiles in the left ventricle (LV) during the progression of heart failure (HF) in the canine tachypacing induced HF model. LV transmural tissue sections were collected at different time points after initiating rapid pacing representing various stages of LV dysfunction, i.e. tachypaced for 3 days (Day-3), 1 week (Week-1), 2 weeks (Week-2), 3-4 weeks (End stage), and unpaced controls (Day-0). As biological replicates, tissues were collected separately from 3 individual dogs at each of the time points. In total we collected 15 tissue samples for all 5 time points. Three RNA samples were independently isolated from each of the 15 tissue samples as technical replicates. The resulting 45 RNA samples were used for microarray experiment. Affymetrix gene expression profiles of the 45 RNA samples were used for all data analysis in this study.
2010-05-19 | E-GEOD-9794 | biostudies-arrayexpress
Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. After administration of C3a receptor (C3aR) antagonist, RV function was dramatically improved PAC-induced RV dysfunction in wild type mice. To investigate the role of C3a to cardiomyocyte, C3a recombinant protein was administerd to neonatal rat ventricular myocytes (NRVMs), the results that several MAP kinesis were phosphorylated by C3a. In turn, to identify the key expressed genes as downstream of C3a in NRVMs, global gene expression analysis was performed in vitro.
2021-09-07 | GSE183503 | GEO
Project description:Analysis of changes of gene expression profiles in the left ventricle (LV) during the progression of heart failure (HF) in the canine tachypacing induced HF model. Gene expression profiling was performed on samples collected at different time points representing various stages of LV dysfunction, i.e. tachypaced for 3 days (Day-3), 1 week (Week-1), 2 weeks (Week-2), 3-4 weeks (End stage), and unpaced controls (Day-0). Results provide insights into molecular mechanisms of heart failure progression. Keywords: time course
2008-09-30 | GSE9794 | GEO
Project description:To characterize a expression patterns in the heart, we used rat. 12 Wistar male rats (8 - 11 weeks) were sacrificed. Left atrium (LA) adjacent to the pulmonary vein (PV), a mass of left ventricle (LV), and free-wall of the right ventricle (RV) was isolated. Each LV mass was dissected into three pieces as samples. Because the SAN isolation procedure takes approximately 20 minutes, SA was isolated separately. The SA region was delimited by the borders of the crista terminalis, the interatrial septum, the superior vena cava, and right atrium (RA). In addition to PV, LV, RV, SA, and RA samples, pulmonary arteries were added to the samples for the rat microarray.
2022-06-22 | GSE203369 | GEO
Project description:Full Title: Transition from Compensated Hypertrophy to Systolic Heart Failure in the Spontaneously Hypertensive Rat: Structure, Function, and Transcript Analysis Gene expression changes and left ventricular remodeling associated with the transition to systolic heart failure (HF) were determined in the spontaneously hypertensive rat (SHR). By combining transcriptomics of left ventricles from six SHR with HF with changes in function and structure we aimed to better understand the molecular events underlying the onset of systolic HF compared to six age-matched, SHR with compensated hypertrophy. Left ventricle (LV) ejection fraction was depressed (82±4 to 52±3 %) in compensated vs. failing animals. Systolic blood pressure decreased and LV end-diastolic and systolic volume increased with HF. Failing SHR hearts also demonstrated increases in left and right ventricular mass relative to non-failing SHRs.  LV papillary muscle force development and shortening velocity decreased, β-adrenergic responsiveness was depressed, myocardial stiffness and myocardial fibrosis increased with HF relative to non-failing animals. Initial micro-array analysis revealed that 1,431 transcripts were differentially expressed with HF compared to non-failing SHR (p<0.05). Of the identified transcripts, lipopolysaccharide binding protein, the most highly expressed transcript with HF, was negatively correlated to myocardial force while elevated expression of the collagen cross-linking enzyme lysyl oxidase correlated positively with muscle stiffness. Besides these individual transcripts, gene set enrichment analysis (GSEA) identified multiple enriched pathways with HF, most prominent of the altered signaling pathways involved TGF-β and insulin signaling. GESA analysis additionally identified altered gene sets involving inflammation, oxidative stress, cell degradation and cell death, among others (all p<0.01). In contrast to diastolic HF where few transcripts are reported to be altered, our data indicate multiple genes and pathways involved in a variety of biological processes characterize the onset of systolic HF, consistent with many functional and structural changes present in the failing hypertensive heart. Comprehensive gene expression profiling of heart failure Rat model vs control.
2010-02-21 | E-GEOD-19210 | biostudies-arrayexpress
Project description:Affymetrix GeneChip Exon-1.0ST was used to study the differential gene profiles in RV (right ventricle) samples from neonates with HLHS (hypoplastic left heart syndrome) versus RV and LV (left ventricle) samples obtained from age-matched controls. Although few significant changes were observed in the genetic profiles between control LV and control RV, many genes passed the false discovery rate in comparing HLHS-RV to RV and LV control groups, with greater differential profiles noted between HLHS-RV and control RV.
2011-12-31 | GSE23959 | GEO
Project description:Right ventricular (RV) failure plays a critical role in any type of heart failure. However, there is no specific therapy developed for RV failure. To understand RV failure, we focused on the RV specific genes. Global gene expression analysis showed that alternative complement pathway-related genes including C3 and Cfd were significantly upregulated in right ventricle in murine heart. We generated the RV failure by right ventricle-specific pressure overload model mice, pulmonary artery constriction (PAC), which induces RV failure around 14 days. In C3 knockout (C3KO) mice, PAC-induced RV dysfunction and fibrosis were significantly attenuated. C3a is produced from C3 by C3 convertase complex including Cfd. Cfd knockout mice also attenuated PAC-induced RV failure. Moreover, C3a receptor (C3aR) antagonist dramatically improved PAC-induced RV dysfunction in wild type mice. Here we revealed the crucial role of C3-Cfd-C3a-C3aR axis in RV failure and highlight the potential therapeutic target for RV failure with no pharmacologic option.
2021-09-07 | GSE183504 | GEO