Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced heart failure effects through novel integrin targeting approach

ABSTRACT: Reduced heart failure effects through novel integrin targeting approach

PROVIDER: PRJNA1037088 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26744800_1.fastq.gz	Fastqsanger.gz
	SRR26744800_2.fastq.gz	Fastqsanger.gz
	SRR26744801_1.fastq.gz	Fastqsanger.gz
	SRR26744801_2.fastq.gz	Fastqsanger.gz
	SRR26744802_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 136

Similar Datasets

Reduced heart failure effects through novel integrin targeting approach

Project description:Heart failure remains one of the largest clinical burdens globally, with little to no improvement in the development of disease-eradicating therapeutics. Integrin targeting has been used in the treatment of ocular disease and cancer, but little is known about its utility in the treatment of heart failure. Here we sought to determine whether the second generation orally available, αvβ3-specific RGD-mimetic, 29P, was cardioprotective. Male mice were subjected to transverse aortic constriction (TAC) and treated with 50μg/kg 29P or volume-matched saline as Vehicle control. At 3 weeks post-TAC, echocardiography showed that 29P treatment significantly restored cardiac function and structure indicating the protective effect of 29P treatment in this model of heart failure. Importantly, 29P treatment improved cardiac function giving improved fractional shortening, ejection fraction, heart weight and lung weight to tibia length fractions, together with partial restoration of Ace and Mme levels, as markers of the TAC insult. At a tissue level, 29P reduced cardiomyocyte hypertrophy and interstitial fibrosis, both of which are major clinical features of heart failure. RNA sequencing identified that, mechanistically, this occurred with concomitant alterations to genes involved molecular pathways associated with these processes such as metabolism, hypertrophy and basement membrane formation. Overall, targeting αvβ3 with 29P provides a novel strategy to attenuate pressure-overload induced cardiac hypertrophy and fibrosis, providing a possible new approach to heart failure treatment.

2024-03-12 | GSE247309 | GEO

SORBS2 regulates integrin-cytoskeleton interactions and extracellular matrix composition in heart failure

Project description:Heart failure is associated with high mortality rates and reduced quality of life. Because of the tight connection between Nppa expression and cardiomyocyte stress, we first determined NPPA correlated genes during heart failure. In this study, we identify SORBS2 as conserved NPPA correlated gene and detail its molecular function and association with heart failure. We used RNA-sequencing on murine whole heart tissue to study the effect of cardiomyocyte-specific genetic loss of Sorbs2 in adult mice in a healthy situation and heart failure model.

2025-03-17 | GSE243463 | GEO

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

SORBS2 regulates integrin-cytoskeleton interactions and extracellular matrix composition in heart failure

Project description:SORBS2 regulates integrin-cytoskeleton interactions and extracellular matrix composition in heart failure

| PRJNA1018537 | ENA

Single nuclei sequencing of human and Mice HFrEF data (Heart Failure with reduced ejection fraction)

Project description:Here we provide snRNA-seq datasets from heart failure patients with reduced ejection fraction and snRNA-SEQ of the corresponding LAD mouse model (permanent ligation of the left anterior descending artery)

2023-08-20 | E-MTAB-13264 | biostudies-arrayexpress

INO80 and heart failure.

Project description:INO80 and heart failure.

| PRJNA1002579 | ENA

Sex differences in skeletal muscle pathology in patients with heart failure and reduced ejection

Project description:Females with heart failure and reduced ejection fraction (HFrEF) have greater physical limitations and a lower quality of life compared to males, however, the role of non-cardiac mechanisms remains poorly resolved. We hypothesized that differences in skeletal muscle pathology between males and females with HFrEF may explain clinical heterogeneity. In this study, we performed an unbiased RNA sequencing of 5 male controls, 5 female controls, 6 male HFrEF patients, and 5 female HFrEF patients.

2024-07-12 | E-MTAB-14110 | biostudies-arrayexpress

Epigenetic gene-expression links heart failure to memory impairment [smallrna_after_saha]

Project description:In current clinical practice care of diseased patients is often restricted to separated disciplines. However, such an organ-centered approach is not always suitable. For example, cognitive dysfunction is a severe burden in heart failure patients. Moreover, these patients have an increased risk for age-associated dementias. The underlying molecular mechanisms are presently unknown and thus corresponding therapeutic strategies to improve cognition in heart failure patients are missing. Using mice as model organisms we show that heart failure leads to specific changes in hippocampal gene-expression, a brain region intimately linked to cognition. These changes reflect increased cellular stress pathways which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Consequently, mice suffering from heart failure exhibit impaired memory function. These pathological changes are ameliorated via the administration of a drug that promotes neuronal euchromatin formation. Our study provides first insight to the molecular processes by which heart failure contributes to neuronal dysfunction and point to novel therapeutic avenues to treat cognitive defects in heart failure patients.

2020-12-01 | GSE159447 | GEO

Epigenetic gene-expression links heart failure to memory impairment [rnaseq_hypoxia_4h]

2020-12-01 | GSE159443 | GEO

Epigenetic gene-expression links heart failure to memory impairment [rnaseq_from_MI_experiment]

2020-12-01 | GSE159442 | GEO