Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of mouse heart after a minimally invasive mitral regurgitation surgery (MiMRS)

ABSTRACT: Mitral valve was damaged to cause regurgitation induced by a novel and minimally invasive surgery in mice, and hearts were collected for high-throughput sequencing at week 2 (compensatory) after surgery.

ORGANISM(S): Mus musculus

PROVIDER: GSE271640 | GEO | 2025/10/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic analysis of mouse heart after a minimally invasive mitral regurgitation surgery (MiMRS)

Project description:Transcriptomic analysis of mouse heart after a minimally invasive mitral regurgitation surgery (MiMRS)

| PRJNA1132674 | ENA

Single-cell analysis reveals the loss of progenitor subpopulation of valvular endothelial cells leads to functional mitral regurgitation

Project description:We conducted single-cell RNA sequencing analysis of mitral valve leaflets extracted from six patients, comprising three individuals with moderate-to-severe functional mitral regurgitation and three nondiseased mitral valve controls. Bioinformatics was used to identify the cell types, describe the cell functions, and investigate cellular developmental trajectories and interactions.

2024-12-27 | GSE241947 | GEO

Transcriptomic analysis of cardiac remodelling following minimally invasive surgery for aortic regurgitation

Project description:Transcriptomic analysis of cardiac remodelling following minimally invasive surgery for aortic regurgitation

| PRJNA1057946 | ENA

mTOR signal in mitral valve diseases

Project description:Mitral valve prolapse (MVP) is often benign but can progress to mitral regurgitation, requiring invasive treatment. In mgR mice with hypomorphic Fbn1 mutations—mimicking Marfan syndrome—myxomatous mitral degeneration and regurgitation develop by 12 weeks. TGF-β and mTOR signaling activation, along with macrophage infiltration, appear by 4 weeks, before histological changes. Short-term rapamycin treatment blocks early TGF-β activation and inflammation, while long-term mTOR or TGF-β inhibition rescues valve degeneration. Transcriptomics revealed integrins as upstream regulators of mTOR. Blocking integrin signaling or altering its pathway prevented mTOR activation. These findings are conserved in human MVP, suggesting that mTOR activation via abnormal integrin-matrix signaling drives disease and that mTOR inhibition may be a potential therapy.

2025-05-07 | GSE293926 | GEO

Transcriptomic analysis of cardiac remodelling following minimally invasive surgery for aortic regurgitation

Project description:To explore the signaling pathways involved in aortic regurgitation (AR)-induced dysregulation from the compensated phase of the heart to the heart failure phase, and to discover the characteristic genes closely related to AR.

2025-11-18 | GSE252164 | GEO

Mitral valve leaflet response to ischemic mitral regurgitation: From gene expression to tissue remodeling

Project description:Mitral valve leaflet response to ischemic mitral regurgitation: From gene expression to tissue remodeling

| PRJNA587626 | ENA

RNA sequencing of rodent myocardial tissue when subjected to mitral regurgitation (MR) for different time-points, compared to normal Sham tissue.

Project description:Purpose: The goal of this study is to compare mRNA related cellular pathways associated with mitral regurgitation compared to Sham Methods: RNA was extracted from myocardial tissue at 2, 10, 20, 40 weeks after MR surgery (n=5 samples/time-point) and was subjected to unbiased RNA sequencing. Conclusions: RNA sequencing revealed an early activation of multiple cellular pathways.

2020-11-30 | GSE148559 | GEO

Exploring Regulatory Mechanisms of Atrial Myocyte Hypertrophy of Mitral Regurgitation through Gene Expression Profiling Analysis: Role of NFAT in Cardiac Hypertrophy

Project description:Regulatory Mechanisms of Atrial Remodeling of Human Mitral Regurgitation

2016-11-07 | GSE63045 | GEO

Differential Requirement for DICER1 Activity during the Development of Mitral and Tricuspid Vlaves

Project description:Mitral and tricuspid valves are essential for unidirectional blood flow in the heart. They are derived from similar cell sources, and yet congenital dysplasia affecting both valves is clinically rare, suggesting the presence of differential regulatory mechanisms underlying their development. We specifically inactivated Dicer1 in the endocardium during cardiogenesis and found that Dicer1-deletion caused congenital mitral valve stenosis and regurgitation, while it had no impact on other valves. We showed that hyperplastic mitral valves were caused by abnormal condensation and extracellular matrix (ECM) remodeling. Our single-cell RNA Sequencing analysis revealed impaired maturation of mesenchymal cells and abnormal expression of ECM genes in mutant mitral valves. Furthermore, expression of a set of miRNAs that target ECM genes was significantly lower in tricuspid valves compared to mitral valves, consistent with the idea that the miRNAs are differentially required for mitral and tricuspid valve development. We thus reveal miRNA-mediated gene regulation as a novel molecular mechanism that differentially regulates mitral and tricuspid valve development, thereby enhancing our understanding of the non-association of inborn mitral and tricuspid dysplasia observed clinically.

2022-08-19 | GSE207226 | GEO

Normal human mitral valve proteome: a preliminary investigation by gel-based and gel-free proteomic approaches

Project description:The mitral valve is a highly complex structure which regulates blood flow from the left atrium to the left ventricle (LV) avoiding a significant forward gradient during diastole or regurgitation during systole. The integrity of the mitral valve is also essential for the maintenance of normal LV size, geometry, and function. Significant advances in the comprehension of the biological, functional, and mechanical behavior of the mitral valve have recently been made. However, current knowledge of protein components in the normal human mitral valve is still limited and complicated by the low cellularity of this tissue and the presence of high abundant proteins from the extracellular matrix. We employed here an integrated proteomic approach to analyse the protein composition of the normal human mitral valve and reported confident identification of 422 proteins, some of which have not been previously described in this tissue. In particular, we described the ability of pre-MS separation technique based on liquid-phase IEF and SDS-PAGE to identify the largest number of proteins. These initial results provide a valuable basis for future studies aimed at analysing in depth the mitral valve protein composition and at investigating potential pathogenetic molecular mechanisms.

2016-08-18 | PXD004397 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data