Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Metabolism Disorder Promotes Isoproterenol-induced Myocardial Injury in Mice with High Temperature and High Humidity and High-Fat Diet

ABSTRACT:

Isoproterenol (ISO) provides a simple and non-invasive method for inducing myocardial injury with lower mortality and higher reproducibility. Phlegm-damp syndrome, as known as “Tanshi” in Chinese, is one of Traditional Chinese Medicine (TCM) syndrome differentiation, which plays an important role in the development of cardiovascular diseases. However, the underlying mechanism remains unknown. In our present study, a myocardial injury mouse model was introduced by ISO administration combined with high temperature and high humidity and high fat diet to simulate phlegm-damp syndrome. Nontargeted metabolomics with LC-MS/MS was adopted to reveal serum metabolism profile for elucidating the possible molecular mechanism.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse phase, Liquid Chromatography MS - positive - reverse phase

SUBMITTER: Taohua Lan

PROVIDER: MTBLS3886 | MetaboLights | 2022-01-10

REPOSITORIES: MetaboLights

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.

Project description:Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. These data show that of new CMs derived from resident c-kitpos eCSCs have a gene expression profile that closely resembles the specific gene expression of adult cardiomyocytes. This result supports a role of c-kitpos eCSCs in the regeneration and repair of myocardial damage. To test the identity and the degree of differentiation of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice. Global gene expression profiles by microarray was obtained in c-kitpos eCSCs, c-kitpos eCSC-derived YFPpos CMs and normal adult CMs. c-kitposCD45neg eCSCs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice and harvested at 4th passage (n=3). YFPpos cardiomyocytes were FACS sorted from left ventricle apex of Lentirius-c-kit/cre recombined B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice 28 days after ISO (N=3). Normal adult CMs were isolated from B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (n=3).

2013-07-30 | E-GEOD-49318 | biostudies-arrayexpress

Differential expression profiles of tsRNAs in myocardial ischemic rats with/without caloric restriction

Project description:We report the application of high-throughput RNA sequencing technology to examine expression profiling of transfer RNA (tRNA)-derived small RNAs (tsRNAs) in a normal control group (Norm group), isoproterenol (ISO)-induced myocardial ischemic group (MI group), and CR-pretreatment plus ISO-induced myocardial ischemic group (CR+MI group). A total of 714 precisely matched tsRNAs were identified in the myocardial tissues from the three groups of rats (701 in Norm, 708 in MI, and 712 in CR+MI). We find that 302 tsRNAs were identified to be notably dysregulated in the MI group: 166 tsRNAs were upregulated while 136 tsRNAs were downregulated compared with those in the Norm group. After CR pretreatment, we identified 136 tsRNAs that were significantly altered compared with those in the MI group: 45 were upregulated while 91 were downregulated. This study provides new ideas for future research on elucidating the mechanisms of CR pretreatment through regulating tsRNAs levels in myocardial ischemic injury.

2020-10-01 | GSE158781 | GEO

Genome-wide gene expression analysis of new cardiomyocytes (CMs) derived from resident c-kitpos endogenous cardiac stem cells (eCSCs) after myocardial injury by Isoproterenol (ISO) in mice.

2013-07-30 | GSE49318 | GEO

Vitamin B12 alleviates myocardial ischemia/reperfusion injury

Project description:To examine the protective effect of B12 on myocardial ischemia/reperfusion injury and figure out the mechanism of B12.

2024-01-01 | GSE225105 | GEO

The BMAL1/HIF2A heterodimer modulates circadian variations of myocardial injury

Project description:Cardiac injury following myocardial infarction exhibits a circadian pattern, yet the underlying mechanism remains unclear. To elucidate genes governing circadian variation of myocardial injury, we conducted transcriptomic profiling of left-ventricular tissues from mice or humans experiencing myocardial injury at different daytimes. Through comprehensive analyses, including transgenic mouse models and functional studies, we identified BMAL1 as a pivotal transcription factor modulating diurnal variation of myocardial injury. Remarkably, we discovered that BMAL1 regulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with HIF2A. Substantiating this finding, we determined the cryo-EM structure of the BMAL1/HIF2F/DNA complex, revealing a previously unknown capacity for structural rearrangement within BMAL1. Furthermore, we confirmed amphiregulin (AREG) as a transcriptional target of the BMAL1/HIF2A heterodimer, critical for modulating circadian variation of myocardial injury. Finally, targeting the BMAL1/HIF2A-AREG pathway via timed AREG administration or enhancing circadian rhythm pharmacologically offered significant cardioprotection, implicating this pathway in treating ischemic heart disease.

2024-03-20 | GSE255307 | GEO

Differential gene expression profiles in peripheral blood in Northeast Chinese Han people with acute myocardial infarction

Project description:The genes had different expression between healthy people and acute myocardial infarction.We aimed to identify the differentially expressed genes involved in acute myocardial infarction in Northeast Chinese Han people. We used microarrays to detail the global programme of gene expression to identify the differentially gene between the patients with acute myocardial infarction and healthy people in Northeast Chinese Han people

2017-04-04 | GSE97320 | GEO

Recombinant human thrombomodulin treatment against endotoxemia-induced myocardial injury

Project description:We made LPS induced myocardial injury model mice, and determined the effect of recombinant human thrombomodulin against myocardial injury.

2022-09-01 | GSE131437 | GEO

Plasma microRNA signatures for perioperative myocardial injury.

Project description:The pathophysiological mechanism(s) underlying PMI remain controversial. Small non-coding molecules that modulate gene expression may enhance the detection of myocardial injury and provide further mechanistic insight. We profiled plasma exosomal microRNA in patients who sustained PMI after elective non-cardiac surgery

2020-07-26 | GSE144777 | GEO

Identification of a SIRT3 activator that alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis

Project description:Sirtuin3 (SIRT3) is well known as a conserved nicotinamide adenine dinucleotide+ (NAD+)-dependent deacetylase located in the mitochondria that may regulate oxidative stress, catabolism and ATP production. Accumulating evidence has recently revealed that SIRT3 plays its critical roles in cardiac fibrosis, myocardial fibrosis and even heart failure (HF) , through its deacetylation modifications. Thus, discovery of SIRT3 activators and elucidating their underlying mechanisms of HF should be urgently needed. Herein, we identified a new small-molecule activator of SIRT3 (named 2-APQC) by the structure-based drug designing strategy. 2-APQC was shown to alleviate isoproterenol (ISO)-induced cardiac hypertrophy and myocardial fibrosis in vitro and in vivo rat models. Importantly, in SIRT3 knockout mice, 2-APQC could not relieve HF, suggesting that 2-APQC is dependent on SIRT3 for its protective role. Mechanically, 2-APQC inhibited the mammalian target of rapamycin-p70 ribosomal protein S6 kinase (p70S6K), c-jun N-terminal kinase (JNK) and transforming growth factor-β (TGF-β)/mothers against decapentaplegic homolog 3 (Smad3) pathways to improve ISO-induced cardiac hypertrophy and myocardial fibrosis. Based upon RNA-seq analyses, we demonstrated that SIRT3-pyrroline-5-carboxylate reductase 1 (PYCR1) axis was closely assoiated with HF. By activating PYCR1, 2-APQC could enhance mitochondrial proline metabolism, inhibited ROS-p38MAPK pathway and thereby protecting against ISO-induced oxidative damage. Moreover, activation of SIRT3 by 2-APQC could facilitate AMPK-Parkin axis to inhibit ISO-induced necrosis. Together, our results demonstrate that 2-APQC is a targeted SIRT3 activator that alleviates myocardial hypertrophy and fibrosis by regulating mitochondrial homeostasis, which may provide a new clue on exploiting a promising drug candidate for the future HF therapeutics.

2024-02-28 | GSE260489 | GEO

Myocardial Injury Caused by Chronic Alcohol Exposure——A Pilot Study Based on Proteomic

Project description:Chronic alcohol exposure can cause myocardial degenerative diseases, manifested as cardiac insufficiency, arrhythmia, etc. These are defined as alcoholic cardiomyopathy (ACM). Alcohol-mediated myocardial injury has previously been studied through metabolomics, and it has been proved to be involved in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway related to the biosynthesis of unsaturated fatty acids and oxidative phosphorylation, which tentatively explored the mechanism of ACM induced by chronic drinking. To further study the myocardial damage caused by alcohol, the mouse model of ACM successfully established previously was used to perform proteomics analysis on myocardial specimens. Fifty-six differentially expressed proteins (DEPs) were identified, and they are involved in the KEGG pathway related to fatty acid biosynthesis, lipid metabolism, oxidative stress, and the development of dilated cardiomyopathy (DCM). The present study further demonstrated the underlying causes of myocardial damage caused by chronic alcohol consumption and lays the foundation for further research to clarify the underlying mechanism of ACM.

2022-08-12 | PXD032949 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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