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Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE240850 | GEO | 2024/08/01

REPOSITORIES: GEO

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Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [CUT&Tag]

Project description:In the present study, the induction of AMI in rats was achieved by ligating the left anterior descending coronary artery (LAD) for a duration of one hour (early time reperfusion, defined as ETR) or six hours (late time reperfusion, and defined as LTR), followed by reperfusion. Sham-operated rats served as controls for the experiment. Bulk tissue transcriptomic sequencing, metabolomic profiling, and single-nucleus RNA sequencing were performed to analyze the transcriptome and metabolome of the ischemic hearts. TF motif analysis was used to predict the potential transcriptional factor. In addition, we investigated the role of ERRβ and ERRγ in vitro using neonatal rat ventricular myocytes (NRVMs) subjected to hypoxia/reoxygenation (H/R). We administered the ERRβ/γ agonist GSK4716 to rats to assess its therapeutic effects on AMI injury, and compared the protective mechanism with fenofibrate.Bulk tissue transcriptomic and metabolomic profiling demonstrated that the protective effect of ETR on AMI is mediated by two major parts of FAO and dedifferentiation. Single-nucleus RNA sequencing revealed four distinct cardiomyocyte subpopulations (CM1-CM4), and ETR attenuated AMI injury by preserving a greater number of sub-injured CM2 and immature-like CM4. In addition, ERRβ/γ was found to regulate the expression of FAO and immature cardiomyocyte signature genes in vivo and in vitro. Notably, pretreatment with the ERRβ/γ agonist GSK4716 significantly enhanced the protective effect of ETR on AMI by activating FAO and immature CM genes. CONCLUSIONS: The findings indicate that the protective effect of early time reperfusion is associated with preserved FAO and dedifferentiation. Activation of ERRβ significantly enhances these protective effects, highlighting the therapeutic potential of ERRβ activation in ameliorating AMI injury. These findings suggest that targeting the ERRβ pathway may provide an effective strategy for the treatment of AMI.

2026-01-06 | GSE314993 | GEO

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [snRNA-seq]

Project description:The rats were subjected to left anterior descending (LAD) coronary artery ligation for 1 hour, 6 hours (MI1h and MI6h) and 24 hours (MI24h) along with Sham controls (Sham), and 1-hour, 6-hour ischemia followed by reperfusion (MI1h/R and MI6h/R, mimicking early time reperfusion (ETR) and late time reperfusion (LTR), respectively) followed by heart tissue collection 24 hours post MI to mimic the MI/R injury in AMI patients.The heart infarct zones (Sham, MI1h/R, MI6h/R and MI24h) were isolated to single-nucleus transcriptome analysis. Collected nuclei for each sample were loaded onto 10X Chrominum platform. We obtained 22,234 cells and 17,003 genes. Five major cell types were identified, which included cardiomyocytes (CMs), endothelial cells (ECs), fibroblasts (FBs), macrophages (MACs) and smooth muscle cells (SMCs).

2024-08-01 | GSE240848 | GEO

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [bulk RNA-seq]

2024-08-01 | GSE240847 | GEO

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury

Project description:Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury

| PRJNA1005550 | ENA

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [CUT&Tag]

Project description:Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [CUT&Tag]

| PRJNA1394215 | ENA

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [snRNA-seq]

Project description:Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [snRNA-seq]

| PRJNA1005555 | ENA

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [bulk RNA-seq]

Project description:Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury [bulk RNA-seq]

| PRJNA1005554 | ENA

Multi-omics profiling of mouse myocardial infarction

Project description:Myocardial infarction (MI), the most severe manifestation of coronary artery disease, is a multifactorial pathophysiologic process. Here, we constructed a MI mouse model through ligation of the proximal left anterior descending coronary artery. Then we detected and analysed multi-omics (transcriptome and proteome) at different time points (Control, 10 mininte, 1 hour, 6 hour, 24 hour and 72 hour) after MI. Immune-related pathway, pyroptosis pathway, and autophagy pathway r were significantly increased after MI.

2021-09-14 | GSE153494 | GEO

The ischemia-enhanced myocardial infarction protection-related lncRNA protects against acute myocardial infarction.

Project description:Long non-coding RNA RP11-64B16.4 (myocardial infarction protection-related lncRNA [MIPRL]) is among the most abundant and the most upregulated lncRNAs in ischemic human hearts. However, its role in ischemic heart disease is unknown. We found MIPRL was conserved between human and mouse and its expression was increased in mouse hearts after acute myocardial infarction (AMI) and in cultured human and mouse cardiomyocytes after hypoxia. The infarcted size, cardiac cell apoptosis, cardiac dysfunction, and cardiac fibrosis were aggravated in MIPRL knockout mice after AMI. The above adverse results could be reversed by re-expression of MIPRL via adenovirus expressing MIPRL. Both in vitro and in vivo, we identified that heat shock protein beta-8 (HSPB8) was a target gene of MIPRL, which was involved in MIPRL-mediated anti-apoptotic effects on cardiomyocytes. We further discovered that MIPRL could combine with the messenger RNA (mRNA) of HSPB8 and increase its expression in cardiomyocytes by enhancing the stability of HSPB8 mRNA. In summary, we have found for the first time that the ischemia-enhanced lncRNA MIPRL protects against AMI via its target gene HSPB8. MIPRL might be a novel promising therapeutic target for ischemic heart diseases such as AMI.

| S-EPMC11234438 | biostudies-literature

From multi-omics approaches to personalized medicine in myocardial infarction.

Project description:Myocardial infarction (MI) is a prevalent cardiovascular disease characterized by myocardial necrosis resulting from coronary artery ischemia and hypoxia, which can lead to severe complications such as arrhythmia, cardiac rupture, heart failure, and sudden death. Despite being a research hotspot, the etiological mechanism of MI remains unclear. The emergence and widespread use of omics technologies, including genomics, transcriptomics, proteomics, metabolomics, and other omics, have provided new opportunities for exploring the molecular mechanism of MI and identifying a large number of disease biomarkers. However, a single-omics approach has limitations in understanding the complex biological pathways of diseases. The multi-omics approach can reveal the interaction network among molecules at various levels and overcome the limitations of the single-omics approaches. This review focuses on the omics studies of MI, including genomics, epigenomics, transcriptomics, proteomics, metabolomics, and other omics. The exploration extended into the domain of multi-omics integrative analysis, accompanied by a compilation of diverse online resources, databases, and tools conducive to these investigations. Additionally, we discussed the role and prospects of multi-omics approaches in personalized medicine, highlighting the potential for improving diagnosis, treatment, and prognosis of MI.

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