Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrative Transcriptomics and Cell Systems Analyses Reveal Protective Pathways Controlled by Igfbp-3 in Anthracycline-Induced Cardiomyocyte Injury

ABSTRACT: Integrative Transcriptomics and Cell Systems Analyses Reveal Protective Pathways Controlled by Igfbp-3 in Anthracycline-Induced Cardiomyocyte Injury

PROVIDER: PRJNA852233 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19802200_1.fastq.gz	Fastqsanger.gz
	SRR19802200_2.fastq.gz	Fastqsanger.gz
	SRR19802201_1.fastq.gz	Fastqsanger.gz
	SRR19802201_2.fastq.gz	Fastqsanger.gz
	SRR19802202_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 100

Similar Datasets

Integrative Transcriptomics and Cell Systems Analyses Reveal Protective Pathways Controlled by Igfbp-3 in Anthracycline-Induced Cardiomyocyte Injury

Project description:Anthracyclines such as doxorubicin (Dox) are effective chemotherapeutic agents, however their use is hampered by subsequent cardiotoxicity risk. Our understanding of cardiomyocyte protective pathways activated following anthracycline-induced cardiotoxicity (AIC) remains incomplete. Insulin-like growth factor binding protein (IGFBP) 3 (Igfbp-3), the most abundant IGFBP family member in the circulation, is associated with effects on the metabolism, proliferation, and survival of various cells. Whereas Igfbp-3 is induced by Dox in the heart, its role in AIC is ill-defined. We investigated molecular mechanisms as well as systems-level transcriptomic consequences of manipulating Igfbp-3 in AIC using neonatal rat ventricular myocytes and human induced pluripotent stem cell-derived cardiomyocytes.

2022-06-28 | GSE206803 | GEO

RNA-seq of danshen injection, astaxanthin and diosmetin for the treatment of anthracycline-induced cardiotoxicity in H9c2 cardiomyocytes

Project description:Doxorubicin (DOX) and other anthracyclines are effective chemotherapeutic agents, however, their use is influenced by the risk of cardiotoxicity. We still have an incomplete understanding of the cardiomyocyte protective pathways activated after anthracycline-induced cardiotoxicity (AIC).Danshen injection (DSI), astaxanthin (AXT) and diosmetin (DMT) are effective in the treatment of cardiovascular diseases, but the mechanism of protection against adriamycin-induced cardiotoxicity is unclear. Here, we performed RNA-seq screening in H9c2 cardiomyocytes to determine the potential protective mechanisms of Danshen injection, astaxanthin and diosmetin against AIC.

2024-10-30 | GSE246548 | GEO

Methodological aspects of µLC-MS/MS for wide-scale proteomic analysis of anthracycline-induced cardiomyopathy

Project description:The effort to utilize microflow liquid chromatography for deep-scale proteomic analysis (µLC-MS/MS) is still growing. In this work, we utilized two-dimensional LC separation and peptide derivatization by tandem mass tag and assessed the capability of µLC-MS/MS to reveal protein changes associated with severe anthracycline-induced cardiomyopathy phenotype in comparison with nLC-MS/MS. Finally, control and rabbit myocardium specimens with experimentally induced anthracycline cardiomyopathy were analysed. Nearly 4000 myocardial proteins were quantified using µLC-MS/MS. In concordance with nLC-MS/MS, data evaluation revealed that severe anthracycline cardiotoxicity phenotype was associated with marked global protein dysregulation. Observed protein dysregulation consisted of profound remodelling of cardiomyocyte sarcomere as well as components of extracellular matrix. Pro-inflammatory proteins and multiple antioxidant proteins were markedly changed, whereas the levels of mitochondrial proteins were declined compared to control myocardium. In this study, µLC-MS/MS was confirmed as a versatile proteomic tool for comprehensive mapping of proteome changes related to anthracycline cardiotoxicity having a great potential to become full-fledged alternative to nLC.

2025-04-30 | PXD047014 | Pride

Activation of the ERRα Transcriptional Pathway Alleviates Anthracycline-induced Cardiotoxicity by Improving Mitochondrial Metabolism

Project description:Anthracycline-induced metabolic remodeling and mitochondrial damage are critical early events that contribute to cardiac dysfunction. However, the gene regulatory pathways governing the derangements in myocardial bioenergetics have not yet been fully delineated. Estrogen-related receptor alpha (ERRα) is a key regulator of energy metabolism, especially in tissues with high energy demands. Here, we demonstrate that ERRα acts as a beneficial modulator of mitochondrial metabolism in anthracycline-induced cardiotoxicity (AIC). ERRα gain-of-function enhances cardiomyocyte metabolism and mitochondrial function, thereby alleviating AIC. Conversely, cardiomyocyte-specific knockdown of ERRα exacerbates mitochondrial bioenergetic collapse and worsens heart failure phenotypes in AIC mice. Additionally, our research identifies a top-ranking isoflavone phytoestrogen as a novel ERRα agonist with favorable pharmacological properties. This compound promotes the transcriptional activity of metabolic genes, representing a significant step toward developing natural ERRα agonists for AIC therapy.

2025-03-12 | GSE291450 | GEO

Activation of the ERRα Transcriptional Pathway Alleviates Anthracycline-induced Cardiotoxicity by Improving Mitochondrial Metabolism

2025-03-07 | GSE291275 | GEO

Myeloperoxidase is a Critical Mediator of Anthracycline-induced Cardiomyopathy

Project description:The anthracycline doxorubicin is a commonly used chemotherapeutic drug that induces cardiomyopathy in almost 10% of patients. The aim of this study was to examine the role of the leukocyte-derived enzyme Myeloperoxidase (MPO) in pathogenesis of anthracycline-induced Cardiomyopathy (AICM). We performed proteomics on whole heart tissue of MPO-deficient mice on C57BL/6J background and wildtype (WT) littermates seven days after intravenous injection of the anthracycline Doxorubicin (20 mg/kg bodyweight, dissolved in saline) or saline (NaCl).

2023-08-30 | PXD037524 | Pride

Identification of novel hyper- or hypo-methylated CpG sites and genes associated with anthracycline-induced cardiomyopathy

Project description:Genome wide DNA methylation profiling of peripheral blood DNA from childhood cancer survivors with and without anthracycline induced cardiomyopathy. DNA methylation status of 850,000 CpG sites was analyzed using the Illumina HumanMethylation EPIC BeadChip arrays. Matched case-control study (COG-ALTE03N1); 52 non-Hispanic White, anthracycline-exposed childhood cancer survivors with cardiomyopathy were matched 1:1 with 52 survivors with no cardiomyopathy. Anthracycline-induced cardiomyopathy is a leading cause of late morbidity in childhood cancers survivors. Aberrant DNA methylation plays a role in de novo cardiovascular disease. Epigenetic processes could play a role in anthracycline-induced cardiomyopathy, but remain unstudied. We sought to examine if genome-wide differential methylation at ‘CpG’ sites in peripheral blood DNA is associated with anthracycline-induced cardiomyopathy. We observed significant differences in DNA methylation between anthracycline-exposed childhood cancer survivors with and without cardiomyopathy, implicating differential DNA methylation in anthracycline-induced cardiomyopathy.

2023-03-31 | GSE224359 | GEO

Genomic predictor of response and survival following neoadjuvant taxane-anthracycline chemotherapy in breast cancer

Project description:This SuperSeries is composed of the following subset Series: GSE25055: Discovery cohort for genomic predictor of response and survival following neoadjuvant taxane-anthracycline chemotherapy in breast cancer GSE25065: Validation cohort for genomic predictor of response and survival following neoadjuvant taxane-anthracycline chemotherapy in breast cancer Refer to individual Series

2011-05-11 | E-GEOD-25066 | biostudies-arrayexpress

Haptoglobin Gene Expression and Anthracycline-related Cardiomyopathy in Childhood Cancer Survivors

Project description:In this study RNA-Seq was performed in anthracycline- exposed childhood cancer survivors who had cardiomyopathy (cases) matched to those without cardiomyopathy (controls) to understand the pathogenesis of anthrcaycline-related cardiomyopathy

2023-01-31 | GSE218276 | GEO

Cardiomyocyte-specific knockout of ADAM17 alleviates doxorubicin-induced cardiomyopathy via inhibiting TNFα-TRAF3-TAK1-MAPK axis

Project description:Doxorubicin as a commonly used anthracycline has become the cornerstone of chemotherapy in a wide range of cancers owing to its high efficacy. However, clinical applications of doxorubicin are limited mainly due to its toxic effects on myocardium but the pathogenic mechanism of doxorubicin-induced cardiomyopathy are poorly understood. ADAM17 is known as tumor necrosis factor α converting enzyme (TACE), and the cleavage of TNF-α by ADAM17 is a prerequisite for pro-inflammatory TNF-α activity, which raises a possibility that inhibition of ADAM17 may exert a beneficial effect on disease processes where TNF-α plays an essential role. Our previous research has shown that cardiomyocyte specific knockout of ADAM17 improves diabetic cardiomyopathy by modulating cardiomyocyte apoptosis. However, the relationship between ADAM17 and doxorubicin-induced cardiomyopathy is unclear.Through RNA sequencing analysis, we observed significant changes in the TNF signaling pathway genes in the heart tissue of mice with or without cardiomyocyte ADAM17 knockout.

2024-09-10 | GSE276325 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data