Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [ATAC-seq]

ABSTRACT: A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [ATAC-seq]

PROVIDER: PRJNA1032056 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26515782_1.fastq.gz	Fastqsanger.gz
	SRR26515782_2.fastq.gz	Fastqsanger.gz
	SRR26515783_1.fastq.gz	Fastqsanger.gz
	SRR26515783_2.fastq.gz	Fastqsanger.gz
	SRR26515784_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma

Project description:A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma

| PRJNA1032073 | ENA

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [RNA-seq]

Project description:The lack of an appropriate preclinical model of metabolic dysfunction-associated steatotic liver disease (MASLD) that recapitulates the whole disease spectrum impedes exploration of disease pathophysiology and the development of effective treatment strategies. Considering the fact that MASLD patients accompanying type 2 diabetes mellitus (T2DM) have high risk of developing metabolic dysfunction-associated steatohepatitis (MASH), advanced fibrosis, and HCC, we treated low-dose streptozotocin (STZ; 40 mg/kg) for 5 consecutive days and subsequently fed a high-fat diet (HFD) to male C57BL/6J mice at 7 weeks of age (STZ+HFD). STZ+HFD mice gradually developed fatty liver, MASH, hepatic fibrosis, and hepatocellular carcinoma (HCC) in the context of metabolic dysfunction. In particular, from 20 weeks of age, MASH was evident, and from 32 weeks of age, advanced fibrosis was developed. At 38 weeks, a proportion of STZ+HFD mice developed HCC, which was subsequently observed in all mice up to 68 weeks of age. Furthermore, the hepatic transcriptomic features of STZ+HFD mice closely reflected those of obese patients with T2DM, MASH and MASLD-related HCC. Notably, dietary changes and tirzepatide administration alleviated MASH, hepatic fibrosis, and hepatic tumorigenesis in STZ+HFD mice. In conclusion, a murine model recapitulating the main histopathologic, transcriptomic, and metabolic alterations observed in MASLD patients with metabolic dysfunction was successfully established.

2024-06-17 | GSE246221 | GEO

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [RNA-seq]

Project description:A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [RNA-seq]

| PRJNA1032104 | ENA

Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.

Project description:A proteomic and peptidomics analysis of serum from patients suffering from metabolic dysfunction-associated steatotic liver disease. Proteomics was performed initially on a set of patients with varying degrees of liver disease. Following close analysis of the results, a peptidomics based analysis was performed and identified significant numbers of degraded and oxidised peptides from apolipoproteins. A more targeted peptidomics analysis was performed on a larger cohort and the oxidation status of small apolipoproteins demonstrated a high accuracy of precision for liver disease diagnosis.

2025-01-21 | PXD052061 | Pride

A Mouse Model for Metabolic Dysfunction-associated Steatotic Liver Disease and Hepatocellular Carcinoma [ATAC-seq]

Project description:The lack of an appropriate preclinical model of non-alcoholic fatty liver disease (NAFLD) that recapitulates the whole disease spectrum impedes exploration of disease pathophysiology and the development of effective treatment strategies. Therefore, we developed new mose model with Streptozotocin (STZ)and high-fat diet (HFD). In breif, male C57BL/6J mice were injected with low-dose streptozotocin (40 mg/kg) for 5 consecutive days beginning at 7 weeks of age and subsequently fed a high-fat diet from week 8 (STZ+HFD) onwards. Hepatic histopathology, transcriptomics, epigenetics, and metabolic phenotypes were evaluated at various time-points. The hepatic transcriptomes of STZ+HFD mice and NAFLD patients with similar liver histopathology were compared. In STZ+HFD mice, dietary changes from HFD to standard chow and administration of tirzepatide, a dual glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 receptor agonist, were introduced to assess the therapeutic efficacy of these interventions. STZ+HFD mice gradually developed fatty liver, non-alcoholic steatohepatitis (NASH), hepatic fibrosis, and hepatocellular carcinoma (HCC) in the context of metabolic dysfunction. In particular, from 32 weeks of age, NASH and advanced fibrosis were evident. At 38 weeks, a proportion of STZ+HFD mice developed HCC, which was subsequently observed in all mice up to 68 weeks of age. Furthermore, the hepatic transcriptomic features of STZ+HFD mice closely reflected those of patients with NASH and NAFLD-related HCC. Notably, dietary changes and tirzepatide administration alleviated NASH, hepatic fibrosis, and hepatic tumorigenesis in STZ+HFD mice. Put together, we established a murine model recapitulating the main histopathologic, transcriptomic, and metabolic alterations observed in NAFLD patients with metabolic dysfunction was successfully established.

2024-06-17 | GSE246213 | GEO

Transcriptional profiling of liver obtained from a mouse model for metabolic dysfunction-associated steatotic liver disease

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent hepatic disorder worldwide and closely associated with type 2 diabetes mellitus (T2DM). The pathogenesis of MASLD is multifaceted and its treatment options are very limited. Consequently, it is urgent to identify novel therapeutic targets and develop effective treatment strategies. RNA sequencing analysis was performed to understand the transcriptomic changes in a mouse model of MASLD.

2025-01-20 | GSE279512 | GEO

Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

Project description:Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

| PRJNA1094958 | ENA

Aging Promotes Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-Organ Dysfunction by Inducing Ferroptotic Stress

Project description:Aging Promotes Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-Organ Dysfunction by Inducing Ferroptotic Stress

| PRJNA1091908 | ENA

Binding of the spike of SARS-CoV-2 to steatotic hepatocytes promotes metabolic dysfunction

Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes a multi-organ damage that includes hepatic dysfunction, which has been observed in over 50% of COVID-19 patients. Liver injury in COVID-19 patients could be attributed to the cytopathic effects induced by the interation between the virus and hepatic cells, exacerbated immune responses or treatment-associated drug toxicity. Here we demonstrate that primary hepatocytes are susceptible to infection in different models: hepatocytes derived from humanized angiotensin-converting enzyme-2 (hACE-2) mice and THLE-2 human cells. Pseudotyped viral particles engineered to express the full-length spike of SARS-CoV-2 and recombinant RBD bind to ACE2 expressed by hepatocytes, promoting metabolic reprogramming towards glycolysis but also mitochondrial dysfunction. In the context of non-alcoholic steatohepatitis (NASH), steatotic hepatocytes derived from hACE2 mice are more vulnerable to infection, as a result of increased expression of ACE2. Metformin, a common therapeutic option for hyperglycemia in type 2 diabetes (T2D) patients, prevents the interaction between the spike of SARS-CoV-2 and steatotic hepatocytes by reducing the expression of hACE2. In summary, we provide evidence that hepatocytes are amenable to SARS-CoV-2 infection and propose metformin as a therapeutic strategy to prevent liver dysfunction caused by SARS-CoV-2 in the context of NASH.

2022-10-14 | PXD035263 | Pride

Metabolic dysfunction-associated steatotic liver disease may increase intrahepatic interferon gene signatures in patients with chronic hepatitis B

Project description:As metabolic dysfunction-associated steatotic liver disease (MASLD) frequently co_x0002_occurs in patients with chronic hepatitis B (CHB), the interplay between these two common liver conditions remains largely unexplored. A recent study suggest that MASH comorbidity can reduce intrahepatic interferon pathway activity and macrophage gene signatures in HBeAg_x0002_negative chronic HBV (ENEG) patients, potentially contributing to persistent infection and fibrosis. However, it remains unclear whether this phenomenon also occurs in MASLD with CHB patients.

2025-01-27 | GSE288077 | 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