Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA814392 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18672502_1.fastq.gz | Fastqsanger.gz | |||
| SRR18672502_2.fastq.gz | Fastqsanger.gz | |||
| SRR18672503_1.fastq.gz | Fastqsanger.gz | |||
| SRR18672503_2.fastq.gz | Fastqsanger.gz | |||
| SRR18672504_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Human engineered heart tissue for analyzing human myocardial fibrosis
| PRJNA982805 | ENA
Project description:Bulk RNA-seq of human engineered heart tissue for analyzing human myocardial fibrosis
| PRJNA982808 | ENA
Project description:Myocarditis is a heart condition that causes inflammation and results in the loss of heart muscle cells, often leading to fibrosis (scarring) of the heart tissue and heart failure. However, the molecular mechanisms underlying immune cell control and maintenance of tissue integrity in the inflamed cardiac microenvironment remain elusive. Based on our finding that bone morphogenic protein-4 (BMP4) serum concentration was reduced in myocarditis patients in combination with comprehensive single cell and single nucleus RNA sequencing analyses of inflamed murine and human myocardial tissue indicated that BMP4 gradients maintain cardiac tissue homeostasis. Indeed, restoration of BMP signaling through antibody-mediated neutralization of the BMP-inhibitors GREM1 and GREM2 reduced CD4+ T cell-mediated myocardial inflammation and blocked disease progression by reduction of adverse fibrotic remodelling. These results unveil a key function of the BMP4-GREM1/2 axis as promising approach for treating myocardial inflammation and the serious complications of cardiac fibrosis and heart failure.
2024-01-16 | E-MTAB-12589 | biostudies-arrayexpress
Project description:Myocarditis is a heart condition that causes inflammation and results in the loss of heart muscle cells, often leading to fibrosis (scarring) of the heart tissue and heart failure. However, the molecular mechanisms underlying immune cell control and maintenance of tissue integrity in the inflamed cardiac microenvironment remain elusive. Based on our finding that bone morphogenic protein-4 (BMP4) serum concentration was reduced in myocarditis patients in combination with comprehensive single cell and single nucleus RNA sequencing analyses of inflamed murine and human myocardial tissue indicated that BMP4 gradients maintain cardiac tissue homeostasis. Indeed, restoration of BMP signaling through antibody-mediated neutralization of the BMP-inhibitors GREM1 and GREM2 reduced CD4+ T cell-mediated myocardial inflammation and blocked disease progression by reduction of adverse fibrotic remodelling. These results unveil a key function of the BMP4-GREM1/2 axis as promising approach for treating myocardial inflammation and the serious complications of cardiac fibrosis and heart failure.
2024-01-16 | E-MTAB-12584 | biostudies-arrayexpress
Project description:Myocarditis is a heart condition that causes inflammation and results in the loss of heart muscle cells, often leading to fibrosis (scarring) of the heart tissue and heart failure. However, the molecular mechanisms underlying immune cell control and maintenance of tissue integrity in the inflamed cardiac microenvironment remain elusive. Based on our finding that bone morphogenic protein-4 (BMP4) serum concentration was reduced in myocarditis patients in combination with comprehensive single cell and single nucleus RNA sequencing analyses of inflamed murine and human myocardial tissue indicated that BMP4 gradients maintain cardiac tissue homeostasis. Indeed, restoration of BMP signaling through antibody-mediated neutralization of the BMP-inhibitors GREM1 and GREM2 reduced CD4+ T cell-mediated myocardial inflammation and blocked disease progression by reduction of adverse fibrotic remodelling. These results unveil a key function of the BMP4-GREM1/2 axis as promising approach for treating myocardial inflammation and the serious complications of cardiac fibrosis and heart failure.
2024-01-16 | E-MTAB-12559 | biostudies-arrayexpress
Project description:Myocardial infarction models developed to understand fibrosis and promote myocardial regeneration towards ischemic heart disease (IHD) is challenged due to the low-throughput nature of in vivo models and the lack of humanized cardiac scarring in the in vitro models. We generated a novel 4D cardiac scarring model (4DCSM) mimicking the IHD in vitro based on the human engineered heart tissue(hEHT). To identify potential signaling dominating the fibrotic process, we characterized transcriptomics of 4DCSM at different scarring stages by single-cell RNA sequencing. Taken together, our dataset is an informative resource to reveal the critical cell-types fate transformation and in fibrotic process and provides potential comparisons with public clinical data cohorts or other MI fibrosis model data.
2023-06-14 | GSE234714 | GEO
Project description:Myocardial infarction models developed to understand fibrosis and promote myocardial regeneration towards ischemic heart disease (IHD) is challenged due to the low-throughput nature of in vivo models and the lack of humanized cardiac scarring in the in vitro models. We generated a novel 4D cardiac scarring model (4DCSM) mimicking the IHD in vitro based on the human engineered heart tissue(hEHT). To identify potential signaling dominating the fibrotic process, we characterized transcriptomics of 4DCSM at different scarring stages by bulk RNA sequencing. Taken together, our dataset is an informative resource to reveal the potential signaling dominating the fibrotic process and provides potential comparisons with public clinical data cohorts or other MI fibrosis model data.
2023-06-14 | GSE234715 | GEO
Project description:Myocardial interstitial fibrosis is a common thread in multiple cardiovascular diseases including heart failure, atrial fibrillation, conduction disease and sudden cardiac death. To investigate the biologic pathways that underlie interstitial fibrosis in the human heart, we developed a machine learning model to measure myocardial T1 time, a marker of myocardial interstitial fibrosis, in 41,505 UK Biobank participants. Greater T1 time was associated with diabetes mellitus, renal disease, aortic stenosis, cardiomyopathy, heart failure, atrial fibrillation, conduction disease and rheumatoid arthritis. Mendelian randomization analysis supported a potential causal role for diabetes mellitus type 1 in myocardial interstitial fibrosis. In genome-wide association analysis, we identified 11 independent loci associated with native myocardial T1 time. The identified loci implicated genes involved in glucose transport (SLC2A12), iron homeostasis (HFE, TMPRSS6), tissue repair (ADAMTSL1, VEGFC), oxidative stress (SOD2), cardiac hypertrophy (MYH7B) and calcium signaling (CAMK2D). Transcriptome-wide association studies highlighted the role of expression of ADAMTSL1 and SLC2A12 in human cardiac tissue in modulating myocardial interstitial fibrosis. Using a TGFβ1-mediated cardiac fibroblast activation assay, we found that 9 out of the 11 genome-wide significant loci comprised genes that exhibited temporal changes in expression and/or open chromatin conformation supporting the biological relevance of these loci to myocardial fibrosis and myofibroblast cell state acquisition. Harnessing machine learning to perform large-scale phenotyping of interstitial fibrosis in the human heart, our results yield novel insights into biologically relevant pathways to myocardial fibrosis and prioritize a number of pathways for further investigation.
2023-03-11 | GSE225336 | GEO
Project description:Ischemic heart disease remains the leading cause of mortality and morbidity worldwide despite improved possibilities in medical care. Alongside interventional therapies, such as coronary artery bypass grafting (CABG), adjuvant tissue-engineered and cell-based treatments can provide regenerative improvement. Unfortunately, most of these advanced approaches require multiple lengthy and costly preparation stages without in turn delivering significant clinical benefit.
Here, we investigated the effect of epicardial matrix patch-encased atrial appendage micrografts (AAMs) in a mouse model of myocardial infarction. The matrix-covered AAM patches salvaged the myocardium from infarction-induced functional tissue loss. Fibrosis was attenuated, and site-targeted proteomics revealed AAM patch-activated pathways for angiogenesis and cardiogenesis. The matrix component of the graft further supports functional myocardial recovery by ventricular unloading.
The composite epicardial matrix graft encasing AAM micrografts delivers effects desirable for adjuvant cardiac therapy preserving functional cardiac tissue and restricting fibrosis after myocardial infarction.
2019-07-23 | MSV000084120 | MassIVE
Project description:Engineered human cardiac tissues have been utilized for various biomedical applications, including drug testing, disease modeling, and regenerative medicine. However, the applications of cardiac tissues derived from human pluripotent stem cells are often limited due to their immaturity and lack of functionality. Therefore, in this study, we established a perfusable culture system based on in vivo-like heart microenvironments to improve human cardiac tissue fabrication. The integrated culture platform of a microfluidic chip and a three-dimensional heart extracellular matrix enhanced human cardiac tissue development and their structural and functional maturation. These tissues were comprised of cardiovascular lineage cells, including cardiomyocytes and cardiac fibroblasts derived from human induced pluripotent stem cells, as well as vascular endothelial cells. The resultant macroscale human cardiac tissues exhibited improved efficacy in drug testing (small molecules with various levels of arrhythmia risk), disease modeling (long QT syndrome and cardiac fibrosis), and regenerative therapy (myocardial infarction treatment). Therefore, our culture system can serve as a highly effective tissue-engineering platform to provide human cardiac tissues for versatile biomedical applications.
2024-02-03 | PXD042077 | Pride