Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomics of liver and PBMCs in alcohol-associated liver disease

ABSTRACT: Transcriptomics of liver and PBMCs in alcohol-associated liver disease

PROVIDER: PRJNA899977 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomics of liver and PBMCs in alcohol-associated liver disease

Project description:Transcriptomics of liver and PBMCs in alcohol-associated liver disease

| PRJNA899978 | ENA

The role of retinoic acid receptor signaling in liver cells during Alcohol-associated liver disease resolution by spatial transcriptomics analysis

Project description:Abstinence is beneficial for patients with alcohol-associated liver disease (ALD), but disease resolution after alcohol cessation occurs slowly and only in a subset of patients. Mechanisms of fibrosis resolution in ALD are not yet fully understood. Previous work highlights the importance of liver niche remodeling around areas of fibrosis that involves protein and metabolite mediated cell-cell crosstalk between hepatocytes and non-parenchymal cells. We aimed to study the mechanisms of ALD resolution using spatial transcriptomics. We found that retinoic acid metabolism strongly associated with improved fibrosis resolution in a mouse model of ALD. In agreement with this finding, mice treated with RAR agonist AM580 after alcohol cessation showed improved fibrosis resolution. Spatial transcriptomics analysis of agonist treated mice and controls suggested that RAR activation dramatically altered liver niches thus promoting pro-resolving changes in liver cells.

2026-03-23 | GSE320403 | GEO

Hepatic NMNAT1 is required to defend against alcohol-associated fatty liver disease

Project description:Nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1), an NAD+ synthetase in Preiss-Handler and salvage pathways, governs nuclear NAD+ homeostasis. This study investigated the role of NMNAT1 on alcohol-associated liver disease (ALD). Decreased NMNAT1 expression and activity were observed in the liver of alcohol-associated hepatitis patients and either liver or primary hepatocytes from ALD mice. F-box and WD repeat domain containing 7 (FBXW7)-regulated interferon regulatory factor 1 (IRF1) ubiquitination degradation contributed to alcohol-inhibited NMNAT1 transcriptional level. Hepatic NMNAT1 knockout aggravated alcohol-induced hepatic NAD+ decline and further hepatic steatosis and liver injury. Metabolomics and transcriptomics interaction revealed that cysteine sulfinic acid decarboxylase (CSAD)-regulated taurine pathway was involved in NMNAT1-disrupted hepatic lipid metabolism in ALD. Hepatic CSAD overexpression or taurine supply attenuated hepatic NMNAT1 knockout-aggravated ALD, respectively. Hepatic NMNAT1 loss inhibited NMN-protected ALD. Replenishing hepatic NMNAT1 reversed liver lipid accumulation in ALD mice. These findings identified NMNAT1 as a promising therapeutic target for ALD.

2025-05-25 | GSE297696 | GEO

Alcohol consumption in metabolic associated liver disease (MASLD)

Project description:Recently, alcohol consumption in metabolic associated steatotic liver disease (MASLD) patients is increasing its incidence. However the pathophysiological mechanisms triggering liver damage in this condition remain unclear. In the present study we aimed to elucidate liver phenotype and gut-liver crosstalk in the context of SLD induced by simultaneous and deleterious association of alcohol and metabolic risk factors.

2026-03-13 | GSE291982 | GEO

Spatial transcriptomics analysis of mouse liver tissue during Alcohol-associated liver disease development and resolution

Project description:Spatial transcriptomics analysis of mouse liver tissue during Alcohol-associated liver disease development and resolution

| PRJNA1298930 | ENA

Alcohol consumption in metabolic associated liver disease (MASLD)

Project description:Alcohol consumption in metabolic associated liver disease (MASLD)

| PRJNA1236286 | ENA

Depletion of Mitochondrial Methionine Adenosyltransferase α1 Triggers Mitochondrial Dysfunction in Alcohol-Associated Liver Disease

Project description:Mitochondrial MATα1 is selectively depleted in alcohol-associated liver disease through a mechanism that involves the isomerase PIN1 and the kinase CK2. Alcohol activates CK2, which phosphorylates MATα1 at Ser114 facilitating interaction with PIN1, thereby inhibiting its mitochondrial localization. Blocking PIN1-MATα1 interaction increased mitochondrial MATα1 levels and protected against alcohol-induced mitochondrial dysfunction.

2022-02-17 | PXD030383 | Pride

Sex specific role of KDM5 demethylases in Alcohol-associated Liver Disease

Project description:Alcohol-associated liver disease (ALD) is a major cause of alcohol related mortality. The specific mechanisms responsible for ALD development and progression are not fully understood, and there is limited therapy for any stage of ALD. Sex differences are often disregarded in in genetic and mechanistic studies. We aimed to take an unbiased approach to define sex specific pathways in livers exposed to alcohol. METHODS: Mice were fed LieberDeCarli alcohol liquid diet for 3 weeks. To identify the role of Kdm5b and Kdm5c we injected mice with AAV-shControl at 2x10^11 gc per mouse or AAV-shKdm5b and AAV-Kdm5c vectors at 10^11 gc per mouse. To assess the role of AhR we injected mice with AAV-shControl or AAV-shAhR vectors at 10^11 gc per mouse. RESULTS: We found several pathways affected by alcohol in sex specific way and identified KDM5 demethylases as contributors to that specificity.

2022-02-08 | GSE195889 | GEO

The role of Cebpb in Alcohol-associated Liver Disease development and resolution

Project description:Abstinence is an important therapeutic intervention for patients with alcohol-associated liver disease (ALD). However, fibrosis improvement after cessation is not uniform and some patients do not improve. We aimed to use scATAC-seq analysis in a mouse model of ALD to define the mechanism of poor ALD resolution. We analyzed differentially accessible regions in livers from control, ALD, or 4 weeks post alcohol cessation mice and identified transcription factors activated in ALD that remained activated after alcohol withdrawal. The top hit was C/EBPβ. We found that hepatocyte specific Cebpb knockout prevented ALD development, while knockout at the time of alcohol cessation promoted fibrosis resolution.

2024-09-12 | GSE276692 | GEO

The Integrated "Multiomics" Landscape at Peak Injury and Resolution From Alcohol-Associated Liver Disease

Project description:To investigate the the liver transcriptome at peak injury and during early and late resolution from alcohol-induced liver injury in mice

2022-06-06 | GSE205484 | GEO

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