Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Non-steroidal mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

ABSTRACT: The objective of this study was to test the novel non-steroidal mineralocorticoid receptor antagonist (MRA) finerenone as a monotherapy in a preclinical Duchenne muscular dystrophy (DMD) model. Microarray was used to detail gene expression differences in ventricular heart tissue from finerenone-treated dystrophin-deficient, utrophin-haploinsufficient Het (utrn+/−; mdx) mice versus untreated Het mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE150302 | GEO | 2020/08/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snATAC-seq]

Project description:Mineralocorticoids play a critical role in maintaining sodium and potassium homeostasis and pathophysiological processes including hypertrophy, inflammation and fibrosis. Mineralocorticoid antagonists (MRAs) have shown to protect from kidney and heart disease, however, their molecular mechanism of action is poorly understood. Here we performed single nuclei and bulk transcriptomics and chromatin accessibility analysis to characterize the mode of kidney protection by steroidal and non-steroidal MRA treatment in a rat model of mineralocorticoid-induced cardiorenal end-organ damage. We define mineralocorticoid sensitive cell types and gene network in the kidney. We show that in diseased kidneys specific proximal tubule cells develop an injured profibrotic phenotype expressing Spp1 and Il34. Nonsteroidal finerenone protects from profibrotic differentiation of proximal tubule cells. Profibrotic gene signature can classify human kidney tissue samples and predict prognosis. Our multi-omics approach elucidates target cell types and potential mechanisms of renal protection by finerenone.

2023-11-17 | GSE183840 | GEO

Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snRNA-seq]

2023-11-17 | GSE183839 | GEO

Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [bulk RNA-seq]

2023-11-17 | GSE183841 | GEO

Expression data from quadriceps of myofiber mineralocorticoid receptor conditional knockout (MRcko)/mdx and myeloid cell MRcko/mdx mice compared to Cre-/mdx control mice

Project description:To identify the gene expression differences in skeletal muscles resulting from conditional knockout of the mineralocorticoid receptor in myofibers and myeloid cells in dystrophin-deficient mdx mice

2024-04-03 | GSE244569 | GEO

Non-steroidal mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

Project description:Non-steroidal mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

| PRJNA631738 | ENA

Transcription profiling of mouse mdx animals expressing high levels of utrophin therapeutic implications for DMD

Project description:Duchenne Muscular Dystrophy (DMD) is a fatal muscle wasting disorder caused by dystrophin deficiency. Previous work suggested that increased expression of the dystrophin-related protein utrophin in the mdx mouse model of DMD can prevent dystrophic pathophysiology. Physiological tests showed that the transgenic mouse muscle functioned in a way similar to normal muscle. More recently, it has become possible to analyse disease pathways using microarrays, a sensitive method to evaluate the efficacy of a therapeutic approach. We thus examined the gene expression profile of mdx mouse muscle compared to normal mouse muscle and compared the data with that obtained from the transgenic line expressing utrophin. The data confirm that the expression of utrophin in the mdx mouse muscle results in a gene expression profile virtually identical to that seen for the normal mouse. This study confirms that a strategy to up-regulate utrophin is likely to be effective in preventing the disease. Experiment Overall Design: Here we have addressed important question of changes in the global gene expression profile of mdx mouse muscle compared to normal mouse muscle and compared the data with that obtained from the transgenic line (fiona) expressing high level of utrophin on mdx background.

2008-06-15 | E-GEOD-7187 | biostudies-arrayexpress

Microarray analysis of mdx mice expressing high levels of utrophin: therapeutic implications for DMD

2008-04-23 | GSE7187 | GEO

Transcription profiling of extraocular, hindlimb and cardiac muscles from dKO and MDX mice

Project description:Comparison by expression profiling of tissue from dKO (utrophin/dystrophin-deficient) and MDX mice at 8 weeks of age. Independent triplicate analyses/strain were done for extraocular, hindlimb, and cardiac muscle.

2007-12-04 | E-GEOD-1463 | biostudies-arrayexpress

Extraocular, hindlimb, and cardiac muscles, comparison of dko and mdx mice (Porter lab)

2004-12-08 | GSE1463 | GEO

Transcription profiling of mouse dystrophin-deficient and dystrophin and utrophin double-deficient animalse crossed with mice with full-length hDMD genes

Project description:Crossing of hDMD mice that contain the full-length 2.3 Mb hDMD gene were crossed with dystrophin-deficient mdx mice and dystrophin and utrophin double-deficient mdx x utrn-/- mice resulted in a full rescue of the dystrophic features of these mice, as concluded from histological analysis. Analysis on Affymetrix gene chips demonstrated that also expression profiles of the dystrophic mice were normalized by crossing with transgenic hDMD mice. This confirms the full functionality of the hDMD transgene in mice. Experiment Overall Design: RNA from gastrocnemius muscle from individual mice was hybridized to Affymetrix U74Av2

2008-06-15 | E-GEOD-6790 | biostudies-arrayexpress

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