Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311228 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. We hypothesized that Intralipid (ITLD) protects the heart in LP rodents against I/R injury. We performed genome-wide expression profiling to identify the underlying mechanisms. Female LP rat hearts were subjected to ischemia followed by reperfusion with vehicle or ITLD (one bolus of 5mg/kg).
2016-02-09 | E-GEOD-77698 | biostudies-arrayexpress
Project description:The heart of late pregnant (LP) rodents is more prone to ischemia/reperfusion (I/R) injury compared to non-pregnant rodents. We hypothesized that Intralipid (ITLD) protects the heart in LP rodents against I/R injury. We performed genome-wide expression profiling to identify the underlying mechanisms.
2016-02-09 | GSE77698 | GEO
Project description:Fibrinogen is upregulated following kidney damage and protects it against ischemia-reperfusion injury
| PRJNA137139 | ENA
Project description:Heart disease remains the leading cause of death globally. Although reperfusion following myocardial ischemia can prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart damage. The mechanisms that drive ischemia/reperfusion injury are not well understood; currently, few methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia. Here, we explored the energetic sustainability of cardiomyocytes, using a model for cellular metabolism to predict the levels of ATP following hypoxia. We modeled glycolytic metabolism with a system of coupled ordinary differential equations describing the individual metabolic reactions within the cardiomyocyte over time. Reduced oxygen levels and ATP consumption rates were simulated to characterize metabolite responses to ischemia. By tracking biochemical species within the cell, our model enables prediction of the cell’s condition up to the moment of reperfusion. The simulations revealed a distinct transition between energetically sustainable and unsustainable ATP concentrations for various energetic demands. Our model illustrates how even low oxygen concentrations allow the cell to perform essential functions. We found that the oxygen level required for a sustainable level of ATP increases roughly linearly with the ATP consumption rate. An extracellular O2 concentration of ~0.007 mM could supply basic energy needs in non-beating cardiomyocytes, suggesting that increased collateral circulation may provide an important source of oxygen to sustain the cardiomyocyte during extended ischemia. Our model provides a time-dependent framework for studying various intervention strategies to change the outcome of reperfusion.
2024-09-02 | BIOMD0000000961 | BioModels
Project description:NTPDase8 protects against liver ischemia-reperfusion injury
| PRJNA1181795 | ENA
Project description:Gene Expression Changes due to Rat Lung Ischemia-Reperfusion Injury
| PRJNA103489 | ENA
Project description:Decorin protects cardiac myocytes against simulated ischemia/reperfusion injury
| PRJEB39277 | ENA
Project description:Mesenchymal stem cells gene expression on liver after ischemia-reperfusion injury.
| PRJNA208663 | ENA
Project description:Time-Dependent miRNA Profiling Following Ischemia/Reperfusion Injury in Rat Retina
| PRJNA260187 | ENA
Project description:<p>Exercise promotes physiological cardiomyocyte growth and protects against ischemia/reperfusion (I/R) injury in the heart. The molecular mechanism by which exercise benefits cardiac metabolism and function remains largely unknown. Using a genetically encoded fluorescent indicator, we found that exercise increased cytosolic, but not mitochondrial, NADPH levels in cardiomyocytes. This effect was mediated by activation of pentose phosphate pathway (PPP). Downregulation of G6PD expression through knocking down transcription factor SP1 or G6PD itself, or depletion of cytosolic NADPH blocked exercise-induced heart hypertrophy. NADPH promoted cardiomyocyte growth through inhibiting HDAC3/C/EBPβ pathways. Moreover, exercise suppressed acute I/R injury and preserved heart function 4 weeks after I/R by mediating G6PD/NADPH pathway. Among 310 Tibetan compounds, lyciumspermidine-0527, a new spermidine derivative, directly activated G6PD, elevated intracellular NADPH levels, promoted cardiomyocytes growth and alleviated I/R injury. PPP-derived NADPH is a critical metabolic checkpoint that regulates exercise-induced physiological cardiomyocyte growth and protects against I/R-induced heart injury.</p>
2026-03-22 | MTBLS14090 | MetaboLights