Cardiac organoid model of human myocardial infarction (batch2)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA473541 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7230170.fastq.gz | Fastqsanger.gz | |||
| SRR7230171.fastq.gz | Fastqsanger.gz | |||
| SRR7230172.fastq.gz | Fastqsanger.gz | |||
| SRR7230173.fastq.gz | Fastqsanger.gz | |||
| SRR7230174.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:While human organoid systems have provided a powerful platform in modeling diseases caused by genetic disorders, non-genetic factors, such as lifestyle and environment, are the largest attributable factors to devastating diseases like cardiovascular disease (CVD), the leading cause of death worldwide. Specifically, myocardial infarction (MI) (i.e., heart attack) makes up ~8.5% of CVD and is a common cause of heart failure with a 40% five-year mortality after the first MI. This highlights an urgent need to develop relevant human heart failure models for drug development. This is further evidenced by the disappointing performance of heart failure drugs in clinical trials during the last decade, which has been partially attributed to the distinct differences between human patient hearts and animal heart failure models. Here, we combined major non-genetic causal factors of MI with our previously established cardiac organoids to create the first human organoid model of cardiac infarction. In particular, we leveraged the diffusion limitation in 3D microtissues to recreate the nutrient diffusion gradient across infarcted hearts (i.e., infarct-border-remote zones) in human cardiac organoids to induce cardiac organotypic response to infarction. This enabled the recapitulation of major MI hallmarks in human cardiac organoids at the transcriptomic, structural and functional level.
2020-04-14 | GSE115031 | GEO
Project description:Cardiac organoid model of human myocardial infarction
| PRJNA454314 | ENA
Project description:While human organoid systems have provided a powerful platform in modeling diseases caused by genetic disorders, non-genetic factors, such as lifestyle and environment, are the largest attributable factors to devastating diseases like cardiovascular disease (CVD), the leading cause of death worldwide. Specifically, myocardial infarction (MI) (i.e., heart attack) makes up ~8.5% of CVD and is a common cause of heart failure with a 40% five-year mortality after the first MI. This highlights an urgent need to develop relevant human heart failure models for drug development. This is further evidenced by the disappointing performance of heart failure drugs in clinical trials during the last decade, which has been partially attributed to the distinct differences between human patient hearts and animal heart failure models. Here, we combined major non-genetic causal factors of MI with our previously established cardiac organoids to create the first human organoid model of cardiac infarction. In particular, we leveraged the diffusion limitation in 3D microtissues to recreate the nutrient diffusion gradient across infarcted hearts (i.e., infarct-border-remote zones) in human cardiac organoids to induce cardiac organotypic response to infarction. This enabled the recapitulation of major MI hallmarks in human cardiac organoids at the transcriptomic, structural and functional level.
2020-04-14 | GSE113871 | GEO
Project description:Mouse myocardial infarction cardiac proteome sequencing
| PXD053227 |
Project description:The aims of the experiment were to profile the cell types in the adult mouse cardiac interstitium (non-myocyte cells) and how they respond to myocardial infarction injury. Adult, male, Pdgfra +/GFP mice were subject to either a myocardial infarction or sham injury, with cells isolated from cardiac ventricles 3 or 7 days following surgery. We obtained scRNA-seq profiles of two cell fractions: total interstitial (non-myocyte) cell population (TIP) and FACS-sorted GFP+/Cd31- cells (GFP).
2019-03-28 | E-MTAB-7376 | biostudies-arrayexpress
Project description:To investigate the transcriotome alteration in myocardial infarction (MI)-associated cells, we performed RNA sequcening analysis with single cells derived from mouse infarcted cardiac tissues or normal left ventricle (LV). Particularly, cardiac endothelial cells (ECs) were traced using a Cdh5-Cre;LSL-tdTomatom system.
2022-03-01 | GSE163956 | GEO
Project description:To investigate the transcriotome alteration in endothelial cells (ECs) under a myocardial infarction (MI) condition, we performed RNA sequcening analysis with sorted ECs derived from mouse infarcted cardiac tissues or normal left ventricle (LV).
2021-12-31 | GSE163772 | GEO
Project description:Introduction: Coronary atherosclerotic heart disease is an important, worldwide burden on human health. Central muscle infarction is the most dangerous condition, has the highest mortality and disability rates, and is gradually becoming more common among young people. After myocardial infarction, neutrophils recruited to the infarcted area promote the myocardial inflammatory response by releasing proinflammatory factors and chemokines and release matrix metalloproteinases and myeloperoxidases that degrade the extracellular matrix and produce reactive oxygen species, resulting in irreversible myocardial damage and thereby promoting ventricular remodeling. Methods: In this study, we constructed a mouse model of myocardial infarction and utilized the CXCR2 receptor inhibitor navarixin (Nav) to reduce neutrophil recruitment after MI. Results: We observed that Nav improved cardiac function, reduced myocardial damage, reduced neutrophil infiltration, reduced inflammatory factor expression and improved cardiac fibrosis in mice. Through transcriptomic analysis, we found that Nav affects signaling pathways such as the innate immune response and the chemokine signaling pathway, thereby decreasing the inflammatory response by reducing neutrophil chemotaxis. Discussion: This study provides new insights for the use of CXCR2 inhibitors as new therapeutic options for myocardial infarction in the future.
2025-03-11 | GSE291292 | GEO
Project description:Myocardial infarction is a leading cause of mortality worldwide 1 . While advances have been made
in acute treatment, an incomplete understanding of remodelling processes has limited the
effectiveness of therapies to reduce late-stage mortality 2 . Here, we generate an integrative high-
resolution map of human cardiac remodelling after myocardial infarction using single-cell gene
expression, chromatin accessibility, and spatial transcriptomic profiling of multiple physiological
zones at distinct time points in myocardium from myocardial infarction and control patients.
Multimodal data integration allowed us to evaluate cardiac cell-type compositions at increased
resolution, yielding insights into changes of the cardiac transcriptome and epigenome through the
identification of distinct tissue structures of injury, repair and remodelling. We identified and
validated disease-specific cardiac cell-states of major cell-types and analysed them in their spatial
context, evaluating their dependency on other cell-types. Our data elucidates molecular principles
of human myocardial tissue organisation, recapitulating a gradual cardiomyocyte and myeloid
continuum following ischemic injury. In total, our study provides an integrative molecular map of
human myocardial infarction and represents an essential reference for the field and paves the way
for advanced mechanistic and therapeutic studies of cardiac disease.
| EGAS00001006330 | EGA
Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs cardiomyocyte regeneration or promotes maladaptive remodeling, leading to compromised cardiac function.
2024-12-02 | E-MTAB-14508 | biostudies-arrayexpress