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Diabetic ischaemic cardiomyopathy: Characterising the left ventricular myocardial molecular profile in advanced human heart failure

ABSTRACT: Diabetic ischaemic cardiomyopathy: Characterising the left ventricular myocardial molecular profile in advanced human heart failure

PROVIDER: PRJNA1096663 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28574100_1.fastq.gz	Fastqsanger.gz
	SRR28574100_2.fastq.gz	Fastqsanger.gz
	SRR28574101_1.fastq.gz	Fastqsanger.gz
	SRR28574101_2.fastq.gz	Fastqsanger.gz
	SRR28574102_1.fastq.gz	Fastqsanger.gz

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Diabetic ischaemic cardiomyopathy: Characterising the left ventricular myocardial molecular profile in advanced human heart failure

Project description:Ischaemic cardiomyopathy (ICM) is the most common cause of heart failure (HF) and often coexists with diabetes mellitus (DM). Yet, their combined effects are seldom investigated and are poorly understood. Herein, we performed multi-omic analyses of end-stage ICM with DM (ICM-DM) against ICM-No DM, non-ischaemic (dilated) cardiomyopathy with DM (NICM-DM), NICM-No DM, and healthy age-matched donors (AMD). Tissue was sourced from pre-mortem human left ventricular myocardium. Though fatty acid oxidation (FAO) proteins were down-regulated in ICM-DM relative to AMD and other HF, the unique ICM-DM down-regulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins indicated FAO may not be entirely impaired. Oxidative phosphorylation appeared reduced in HF but exacerbated in ICM-DM, consistent with purportedly increased oxidative stress. Extracellular matrix proteins including collagens were up-regulated principally in ICM-DM despite the absence of macroscopic scar tissue. These findings were supported histologically and in metabolomic and RNA sequencing analyses.

2025-04-04 | GSE263297 | GEO

Diabetic ischaemic cardiomyopathy: Characterising the left ventricular myocardial molecular profile in advanced human heart failure

Project description:Ischaemic cardiomyopathy (ICM) is the most common cause of heart failure (HF) and often coexists with diabetes mellitus (DM). Yet, their combined effects are seldom investigated and are poorly understood. We performed multi-omic analyses of end-stage ICM with DM (ICM-DM), ICM-No DM, non-ischaemic cardiomyopathy with DM (NICM-DM), and NICM-No DM against healthy age-matched donors (AMD). Tissue was sourced from pre-mortem human left ventricular myocardium. Though fatty acid oxidation proteins were down-regulated in ICM-DM relative to AMD and other HF conditions, the unique ICM-DM down-regulation of acylcarnitines, perilipin, and ketone body, amino acid, and glucose metabolising proteins indicated lipid metabolism may not be entirely impaired. Oxidative phosphorylation appeared exacerbated in ICM-DM, consistent with purportedly increased oxidative stress. Extracellular matrix proteins were up-regulated principally in ICM-DM despite the absence of scar tissue. These findings indicate DM confounds the pathological phenotype in HF, and the need for a paradigm shift regarding lipid metabolism.

2025-07-02 | PXD052878 | Pride

Molecular remodeling of ion channels, exchangers and pumps in atrial and ventricular myocytes in ischemic cardiomyopathy: left ventricle DCM

Project description:We wanted to see whether the set of affected genes in ischemic cardiomyopathy (ICM) is the same or different as compared to dilated cardiomyopathy (DCM). To find this out, we placed the single DCM sample on the same microarray slide with the ICM samples. Analysis of microarray data with ICM samples only showed 63 affected genes, while that carried out with 2 ICM samples PLUS one DCM sample reduced this number to just four genes. From this result we conclude that ICM and DCM affect different sets of genes in ventricular myocytes. Keywords: Expression profiling by array From the associated publication: To find out whether the splice microarray results reported in Table 3 are disease-type specific, we supplemented the same splice microarray of ICM ventricular myocytes with one additional sample prepared from left ventricle of a 41-years old dilated cardiomyopathy male donor. The top-list ANOVA gene score annotation for combined altered CE&P genes in ventricular myocytes (Table 3) was reduced from 63 to just 4 genes (FXYD1 (Gfold = +2.4), HCN2 (-1.5), GLRA1 (-1.8) and GJC1 (-2.3)).

2010-06-17 | E-GEOD-17530 | biostudies-arrayexpress

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

Project description:Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy primarily of the right ventricle characterized through fibrofatty replacement of cardiomyocytes. The genetic etiology in ARVC patients is most commonly caused by dominant inheritance and high genetic heterogeneity. Though histological examinations of ARVC affected human myocardium reveals fibrolipomatous replacement, the molecular mechanisms leading to loss of cardiomyocytes are largely unknown. We therefore analyzed the transcriptomes of 6 ARVC specimen derived from heart transplantation candidates and compared our findings to 6 non-failing donor hearts (NF) which could not be transplanted for technical reasons. In addition, we compared our findings to 7 hearts from patients with idiopathic dilated cardiomyopathy. From each heart left (LV) and right ventricular (RV) myocardial samples were analyzed by Affymetrix HG-U133 Plus 2.0 arrays, adding up to six sample groups. Unsupervised cluster analyses of the six sample groups revealed a clear separation of NF and cardiomyopathy samples. However, in contrast to the other samples, unsupervised cluster analyses revealed no distinct expression pattern in LV and RV samples from ARVC-hearts. We further identified differentially expressed transcripts using t-tests and found transcripts separating diseased and NF ventricular myocardium. Of note, in failing myocardium only about 15-16% of the genes are commonly regulated compared to NF samples. In addition both cardiomyopathies are clearly distinct on the transcriptome level. Comparison of the expression patterns between the failing RV and LV using a paired t-test revealed a lack of major differences between LV and RV gene expression in ARVC hearts. Microarrays were used to elucidate the differences between non-failing control hearts and those, suffering from arrhythmogenic right ventricular cardiomyopathy (ARVC).

2011-11-30 | E-GEOD-29819 | biostudies-arrayexpress

Ventricle-specific myocardial protein and metabolite characterisation in healthy humans, with differential regulation in end-stage cardiomyopathies

Project description:The left and right ventricles of the human heart are functionally and developmentally distinct such that genetic or acquired insults can cause dysfunction in one or both ventricles resulting in heart failure. First, we performed unbiased quantitative mass spectrometry on the myocardium of 25-27 pre-mortem cryopreserved non-diseased human hearts to compare the metabolome and proteome between the normal left and right ventricles. Constituents of gluconeogenesis, glycolysis, lipogenesis, lipolysis, fatty acid catabolism, the citrate cycle and oxidative phosphorylation were down-regulated in the left ventricle, while glycogenesis, pyruvate and ketone metabolism were up-regulated. Inter-ventricular significance of these metabolic pathways was then found to be diminished within end-stage dilated cardiomyopathy and ischaemic cardiomyopathy (n = 30-33), while heart failure-associated pathways were increased in the left ventricle relative to the right within ischaemic cardiomyopathy, such as fluid sheer-stress, increased glutamine to glutamate ratio, and down-regulation of contractile proteins indicating a left ventricular pathological bias.

2024-11-06 | PXD042155 | Pride

Next Generation Sequencing Facilitates Quantitative Analysis of Hypertrophic Cardiomyopathy/Healthy control Left Ventricular Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Hypertrophic Cardiomyopathy/Healthy control Left Ventricular Transcriptomes

| PRJNA789827 | ENA

Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

Project description:Human left ventricular free wall heart tissue was obtained from end-stage heart failure patients at the moment of heart transplantation

2018-03-08 | GSE111544 | GEO

Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

Project description:Whole human genome expression analysis on left ventricular free wall heart tissue samples (Dilated Cardiomyopathy)

| PRJNA437329 | ENA

Myocardial transcriptome analysis of human arrhythmogenic right ventricular cardiomyopathy (ARVC)

2011-11-30 | GSE29819 | GEO

Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy

Project description:Left ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.

2015-08-10 | E-GEOD-71912 | biostudies-arrayexpress

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