Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

ABSTRACT: Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

PROVIDER: PRJNA1037131 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26729722_1.fastq.gz	Fastqsanger.gz
	SRR26729722_2.fastq.gz	Fastqsanger.gz
	SRR26729723_1.fastq.gz	Fastqsanger.gz
	SRR26729723_2.fastq.gz	Fastqsanger.gz
	SRR26729724_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Colchicine Ameliorates Doxorubicin Cardiotoxicity Via Promoting Autophagic Flux

Project description:Doxorubicin (DOX) cardiotoxicity is an important factor of heart failure. The only clinically approved drug is dexrazoxane, while its side effect of secondary malignancies severely limited its application. It is urgent to find other alternative efficacious molecular for these chemotherapy patients. Colchicine is a safe and well tolerated anti-inflammation drug which also functions in attenuating the reactive oxygen species (ROS) generation. High dose of colchicine was reported block the autophagosome-lysosome fusion in cancer cells due to its destabilization effect to the microtubule system, while how colchicine affects the autophagic flux in cardiomyocytes is largely unknown. Recent years low dose of colchicine administration was reported helpful to the patients with pericarditis, postprocedural atrial fibrillation and coronary artery disease, most of the research attributed it to its anti-inflammation effect. Whether the autophagic flux regulated by colchicine also benefits to DOX induced heart failure remains unclear. Doxorubicin (DOX) administration was used to establish heart failure models in vivo and in vitro. Results showed that DOX blocked the autophagic vacuoles degradation, leading to damaged mitochondria and ROS accumulation. Heart failure characteristics were obviously improved after low dose of colchicine administration. Mechanistically, low dose of colchicine promoted the autolysosome degradation, cleared the damaged mitochondria, and ROS accumulation induced by the DOX and as a result attenuated DOX cardiotoxicity.

2024-06-20 | GSE247345 | GEO

Miz1 is required to maintain autophagic flux

Project description:Miz1 is required to maintain autophagic flux

| PRJNA210788 | ENA

Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

| PRJNA1005939 | ENA

Deubiquitinase OTUB1 regulates doxorubicin-induced cardiotoxicity

Project description:Wild-type (WT) and Otub1-heterozygously knock-out mice were applied in the study. Doxorubicin (DOX)-induced subacute cardiotoxicity mouse model was established by 6 intraperitoneal injections during a 2-week period. The differentially expressed genes were analyzed by RNA-sequencing and clustering analyses.

2024-08-16 | GSE240959 | GEO

Targets of miR-212/132 in doxorubicin-induced cardiotoxicity

Project description:We overexpressed miR-212/132 by AAV9 in mouse model of doxorubicin-induced cardiotoxicity and wanted to identify myocardial targets of miR-212/132 in this model.

2018-12-29 | GSE121965 | GEO

Identifying metabolic adaptations of rat cardiomyocytes in response to cardiotoxicity

Project description:Improvements in the diagnosis and treatment of cancer has revealed the long-term side effects of chemotherapeutics, particularly cardiotoxicity. Current clinical measures to track cardiotoxicity are insufficient to diagnose damage before it has been done, necessitating new, early biomarkers of cardiotoxicity. Here, we collected paired transcriptomics and metabolomics data characterizing in vitro cardiotoxicity to three compounds: 5-fluorouracil, acetaminophen, and doxorubicin. Standard gene enrichment and metabolomics approaches identify some commonly affected pathways and metabolites but are not able to readily identify mechanisms of cardiotoxicity. Here, we integrate this paired data with a genome-scale metabolic network reconstruction (GENRE) of the heart to identify shifted metabolic functions, unique metabolic reactions, and changes in flux in metabolic reactions in response to these compounds. Using this approach, we are able to confirm known mechanisms of doxorubicin-induced cardiotoxicity and provide hypotheses for mechanisms of cardiotoxicity for 5-fluorouracil and acetaminophen.

2021-06-01 | GSE166957 | GEO

CRISPRi/a screen of doxorubicin induced cardiotoxicity

Project description:CRISPRi/a screen of doxorubicin induced cardiotoxicity

| PRJNA1155211 | ENA

Transcriptomic analysis of folic acid effects in doxorubicin-induced cardiotoxicity

2015-11-12 | GSE64476 | GEO

Transcriptomic analysis of folic acid effects in doxorubicin-induced cardiotoxicity

Project description:Doxorubicin (DOXO), a chemotherapeutic drug, is cardiotoxic. We hypothesized that folic acid is an effective therapeutic agent in a mouse model of DOXO-induced cardiotoxicity. We performed genome-wide expression profiling to identify the underlying mechanisms. Male C57Bl6 2-mo old mice received DOXO (1x20 mg/kg, ip) or saline (sham). FA (10 mg/d) or placebo (plac) was administered 7d before DOXO administration until the end of the experiment (10d).

2015-11-12 | E-GEOD-64476 | biostudies-arrayexpress

Transcriptional analysis of doxorubicin-induced cardiotoxicity

Project description:Doxorubicin (Dox) is an effective chemotherapeutic agent against a broad range of tumors. However, a threshold dose of doxorubicin causes an unacceptably high incidence of heart failure and limits its clinical utility. We have established two models of doxorubicin cardiotoxicity in mice: 1) in an acute model, mice are treated with 15mg/kg of doxorubicin once; 2) in a chronic model, they receive 3mg/kg weekly for the first 12 of a total of 18 weeks. Using echocardiography, we have monitored left ventricular function of the mouse hearts during treatment in chronic model and seen the expected development of dilated cardiomyopathy (DCM). Treated mice showed histological abnormalities similar to those seen in patients with doxorubicin cardiomyopathy. To investigate transcriptional regulation in these models, we used a microarray we generated with over 5000 independent cDNA clones from murine heart and skeletal muscle. We have identified genes that respond to doxorubicin exposure in both model systems, and confirmed these results using real-time PCR. In the acute model, a set of genes is regulated early and rapidly returns to baseline levels, consistent with the half-life of doxorubicin. In the chronic model, which mimics the clinical situation much more closely, we identified dysregulated genes that implicate specific mechanisms of cardiac toxicity and may serve as biomarkers of doxorubicin induced dilated cardiomyopathy. Keywords: time course

2005-07-22 | GSE2965 | 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