Mouse myocardial infarction
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE314681 | GEO | 2026/01/04
REPOSITORIES: GEO
Similar Datasets
Project description:To explore the differences in the expression of circRNA in myocardial ischemia-reperfusion injury and the potential effects of these differences in circRNA. Methods 6 SPF male SD rats were randomly divided into two groups, including 3 in Myocardial ischemia reperfusion group and 3 threading without ligation in control group by ligating the left anteriors branch for 40 minutes and reperfusing for 2 hours to establish a model of myocardial ischemia reperfusion injury. The myocardial specimens from the infarct area were taken for high-throughput sequencing analysis to obtain differently expressed circRNA. After that, GO and KEGG analysis were performed to speculate on the biological functions and possible biological pathways involved. RT-qPCR was used to verify the sequencing results of differential circRNA, and bioinformatics analysis predicted that circRNA could combine with miRNA to construct a visual network diagram and their interaction. Results Analyzing of 13576 circRNAs detected in 6 rats from MIRI group and control group, A total of 132 circRNAs showed significant differential expression, of which 82 were up-regulated and 50 were down-regulated. The results of GO and KEGG analysis suggest that differential circRNA is closely related to myocardial ischemia reperfusion injury, and KEGG analysis suggests that differential circRNA is involved in calcium, AMPK, mTOR and adrenaline signal pathways. 4 circRNAs were extracted from the up-regulated circRNA for RT-qPCR verification, and the results of 2 were consistent with the high-throughput sequencing results. circRNA-miRNA interaction analysis shows that circRNA interacts with a variety of miRNAs. Conclusions The expression of circRNA in myocardial reperfusion injury rats is significantly different, which may be involved in the occurrence and development of myocardial ischemia-reperfusion injury through miRNA sponge action of circRNA.
2022-06-30 | GSE207093 | GEO
Project description:Ischemia reperfusion injury (IRI) following intervention for myocardial infarction remains an unmet clinical problem. Using an established mouse model, we demonstrated that IRI induces multiple cardiac cell linages to senescence. Senescence is is detrimental to recovery, as treatment with the senolytic navitoclax improves functional recovery.Here we are using SWATH-MS to investigate the molecular mechanisms responsible for the effect of navitoclax treatment.
2020-02-29 | MSV000085040 | MassIVE
Project description:Background: Ischemic preconditioning (IPC), i.e., brief periods of ischemia, protect the heart from subsequent prolonged ischemic injury, and reduces infarction size. Myocardial stunning refers to transient loss of contractility in the heart after myocardial ischemia that recovers without causing permanent damage. The relationship between IPC and myocardial stunning remains incompletely understood. Purpose: The primary aim of this study was to examine the effects of IPC on the relationship between ischemia duration, stunning, and infarct size in an ischemia-reperfusion injury model. The secondary aim of the study was to examine to which extent the phosphoproteomic changes induced by IPC relate to myocardial contractile function. Methods: Rats were subjected to different durations of left anterior descending artery (LAD) occlusion, with or without preceding IPC. Echocardiograms were acquired at 4 and 48 hours to assess cardiac contraction in the affected myocardial segment. Reversible akinesia was defined as the presence of myocardial akinesia at 4 hours that resolved by 48 hours; and was considered to represent myocardial stunning. Infarction size was evaluated using triphenyl tetrazolium chloride staining. Phosphoproteomic analysis was performed in heart tissue from preconditioned and non-preconditioned animals using nano-liquid chromatography-mass spectrometry. Results: Reversible akinesia was observed in a majority of the rats that were subjected to IPC and subsequently exposed to ischemia of 13.5 or 15 minutes of ischemia (83.3% [n/N] and 66.6% [n/N] respectively). Among rats without IPC, who were exposed to either 10, 11, 12 or 13.5 minutes of ischemia, reversible akinesia was observed in 0% (n/N), 17% (2/12), 0% (n/N) and 0% (n/N) of rats (p<0.001). Phosphoproteomic analysis revealed significant differential regulation of 809 phosphopeptides between IPC and non-IPC groups, with significant associations with the sarcomere, Z-disc, and actin binding. Conclusion: Our study shows that IPC preferentially induces changes in phosphosites of proteins involved in myocardial contraction, and both increases the incidence of reversible post-ischemic myocardial stunning after ischemia-reperfusion injury and reduces infarction size.
2024-05-15 | PXD050441 | Pride
Project description:Myocardial infarct size (IS) and now reflow are major determinants of prognosis and currently there are no effective treatments. We investigated the effects of empagliflozin on cardiac cell populations affected by myocardial ischemia reperfusion injury (IRI), and its cardioprotective potential in terms of IS and no-reflow.
2024-09-13 | GSE255933 | GEO
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:Post-injury remodeling is a complex process involving temporal specific cellular interactions in the injured tissue where the resident fibroblasts play multiple roles, including inflammation induction and tissue remodeling. To dissect the molecular basis of these interactions, we performed single-cell and spatial transcriptome analysis in human and mouse hearts after myocardial infarction. A subset of fibroblasts identified by unique high expression of CD248 was strongly correlated with collagen synthesis and remodeling, and genetic deletion of CD248 in fibroblast ameliorated cardiac fibrosis and dysfunction following ischemia/reperfusion, highlighting the functional importance of CD248 positive fibroblasts in post-injury pathological remodeling. CD248 stabilizes TGF-βR Ⅰ protein and activates ACKR3 expression in fibroblast, leading to enhanced T cell adhesion and retention. This CD248 mediated fibroblast-T cell interaction is required to sustain fibroblast activation and scar expansion in injured heart. Disruption of this interaction using monoclonal antibody or Chimeric antigen receptor T cell reduces T cell infiltration, ameliorates ischemia/reperfusion-induced cardiac fibrosis and improves heart function. Therefore, single cell molecular profiling in post-injury heart has uncovered a CD248 specific subclass of fibroblast with a critical role in fibroblast-T cell interaction and a new potential therapy to treat tissue fibrosis.
2025-02-03 | GSE288103 | GEO
Project description:Aims: Mesenchymal stem cells (MSCs) gradually become attractive candidates for cardiac inflammation modulation, yet understanding of the mechanism remains elusive. Strikingly, recent studies indicated that exosomes secreted by MSCs might be a novel mechanism for the beneficial effect of MSCs transplantation after myocardial infarction. We therefore explored the role of MSC-derived exosomes (MSC-Exo) in the immunomodulation of macrophages after myocardial ischemia-reperfusion and its implications in cardiac injury repair. Methods and Results: Exosomes were isolated from the supernatant of MSCs using a gradient centrifugation method. Administration of MSC-Exo through intramyocardial injection after myocardial ischemia reperfusion reduced infarct size and alleviated inflammation level in heart and serum. Systemic depletion of macrophages with clodronate liposomes abolished the curative effects of MSC-Exo. MSC-Exo modified the polarization of M1 macrophages to M2 macrophages both in vivo and in vitro. miRNA-sequencing of MSC-Exo and bioinformatics analysis implicated miR-182 as a potent candidate mediator of macrophage polarization and TLR4 as a downstream target. Diminishing miR-182 in MSC-Exo partially attenuated its modulation of macrophage polarization. Likewise, knock down of TLR4 also conferred cardioprotective efficacy and reduced inflammation level in a mouse model of myocardial ischemia/reperfusion. Conclusion: Our data indicates that MSC-Exo attenuates myocardial ischemia/reperfusion injury via shuttling miR-182 that modifies the polarization state of macrophages. This study sheds new light on the application of MSC-Exo a potential therapeutic tool for myocardial ischemia/reperfusion injury.
2021-09-01 | GSE120149 | GEO
Project description:The circRNA array was applied to investigate the expression level of circRNAs in the blood samples of coronary arteries of AMI patients and normal persons. Differentially-expressed circRNAs and potential circRNA-miRNA networks were identified in AMI patients.
2020-11-04 | GSE160717 | GEO
Project description:Background. Ischemic preconditioning (IPC) reduces infarct size but may increase the extent of reversible cardiac dysfunction (myocardial stunning). DNA methylation is thought to regulate IPC-induced gene expression, impacting inflammation, oxidative stress, apoptosis, and DNA repair pathways. Aims. This study aimed to identify transcriptomic changes associated with IPC and elucidate the role of DNA methylation in regulating these changes, thereby distinguishing the mechanisms underlying IPC-mediated protection from necrosis and myocardial stunning. Methods. A rat model of cardiac ischemia-reperfusion (I/R) injury was used, with IPC induced by two 5-minute ischemia-reperfusion cycles followed by 13.5 minutes of ischemia, and a control group undergoing 13.5 minutes of ischemia without IPC. Myocardial samples were collected at early (T1) and 4-hour (T2) post reperfusion, representing stunned myocardium in the IPC group and necrosis in the control group. RNA sequencing, DNMT activity assay and promoter methylation analyses of differentially expressed genes (DEGs) were performed to assess transcriptomic and epigenetic changes. Results. IPC reprogrammed the cardiac transcriptome, with 53 DEGs at T1 and 166 at T2, including key regulators of inflammation (Nfkbia), DNA repair (Gadd45b), and stress responses (Cebpd, Jun). Long non-coding RNAs (lncRNAs) were also enriched. IPC reduced global DNMT activity, promoting hypomethylation of protective genes such as Cebpd, Nfkbia, Gadd45b, Jun, and Aplod1 at T1, while selectively hypermethylating maladaptive genes like Tmem200c and Fgfr4 despite persistent reduced global DNMT activity at T2. Conclusion. IPC reprograms the cardiac transcriptome through dynamic DNA methylation changes, potentially mediating protection against myocardial necrosis as an adaptive response.
2025-12-02 | GSE284606 | GEO
Project description:Purpose：Detection of differentially expressed lncRNA in the infarct zone and the control group in myocardial ischemia-reperfusion injury model tissue. Method: Use 8 weeks of C57BL/6 mice to establish a myocardial ischemia-reperfusion injury model, 45 minutes of ischemia, and 24 hours after reperfusion, the mice were sacrificed to obtain materials. Result: The expression of lncRNAs in the infarct area of myocardial ischemia-reperfusion injury model mice was detected, and it was found that a total of 43 lncRNAs related to myocardial ischemia-reperfusion injury changed in expression, of which 17 were up-regulated (fold change >1.5). 26 expressions are down-regulated (fold change <0.8)
2020-11-11 | GSE161151 | GEO