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Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution II

ABSTRACT: Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution II

PROVIDER: PRJNA1124907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29436100_1.fastq.gz	Fastqsanger.gz
	SRR29436100_2.fastq.gz	Fastqsanger.gz
	SRR29436200_1.fastq.gz	Fastqsanger.gz
	SRR29436200_2.fastq.gz	Fastqsanger.gz
	SRR29436101_1.fastq.gz	Fastqsanger.gz

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Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution

Project description:Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution

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Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution I

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Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution I

Project description:Alcohol-associated hepatitis (AH) is an acute form of alcohol-related liver disease (ArLD) with high mortality rate. AH is histologically characterised by cellular processes including steatosis, inflammation and cell death. Apoptosis is the most studied form of cell death in AH; however, the role of cellular senescence, another response to cellular injury, in AH is unknown. Here we aim to explore the mechanisms of ArLD pathophysiology and define the role of senescence in AH.

2025-03-28 | GSE269566 | GEO

Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution II

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CXCR4 DRIVES HEPATOCYTE REPROGRAMMING IN ALCOHOL-RELATED LIVER DISEASE

Project description:Backgruound and aims: Loss of hepatocyte identity is associated with impaired liver function in alcohol-related hepatitis (AH). However, the mechanisms and the impact of hepatocyte reprogramming in liver disease are poorly understood. Here we show that both hepatocytes expressing KRT7 (hepatobiliary (HB) cells) and ductular reaction cells were increased in decompensated cirrhotic patients and AH, but only HB cells correlated with poor liver function, reduced liver synthetic capacity and poor outcome. Transcriptomic analysis of microdissected HB cells revealed the expression of biliary-specific genes and a mild reduction of hepatocyte metabolism. Functional analysis identified pathways involved in hepatocyte reprogramming together with inflammatory, stemness and cancer gene programs. In this context, CXCR4 pathway was highly enriched in HB cells, and CXCR4 correlated with disease severity and reduced expression of hepatocyte transcription factors and albumin. Mechanistically, TGFβ induced the expression of CXCR4 in primary hepatocytes, and its ligand CXCL12 promoted hepatocyte reprogramming. Liver overexpression of CXCR4 in chronic liver injury decreased hepatocyte gene expression and promoted liver injury. Pharmacological inhibition of CXCR4 reverted hepatocyte loss of identity and reduced ductular reaction and fibrosis progression. Conclusions: This study shows the association of hepatocyte reprogramming with disease progression and poor outcome in AH. Moreover, we identify CXCR4 as a driver of hepatocyte reprogramming as well as a potential therapeutic target in chronic liver injury.

2023-04-06 | GSE199168 | GEO

The extent of liver injury determines hepatocyte fate toward senescence or cancer

Project description:Induction of hepatocyte senescence is known to inhibit hepatocellular carcinoma (HCC). Until now, it has not been clear how the degree of liver injury dictates hepatocyte senescence and carcinogenesis. In this study, we investigated whether the severity of injury determines cell fate decisions between hepatocyte senescence and carcinogenesis. After testing of different degrees of liver injury, we found that hepatocyte senescence is strongly induced in the setting of severe acute liver injury. Longer-term, moderate liver injury did not result into hepatocyte senescence, but instead led to a significant incidence of HCC. In addition, carcinogenesis was significantly reduced by the induction of severe acute injury after chronic moderate liver injury. We conclude that severe acute liver injury leads to hepatocyte senescence along with a low incidence of HCC, whereas chronic moderate injury allows hepatocytes to proliferate rather than to enter into senescence, and correlates with a high incidence of HCC. This study improves our understanding in hepatocyte cell fate decisions and suggests a potential clinical strategy to induce senescence to treat HCC.

2018-12-20 | GSE108328 | GEO

Exome sequencing of Alcohol-associated Hepatitis

Project description:Exome sequencing of Alcohol-associated Hepatitis

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Exome sequencing of Alcohol-associated Hepatitis

Project description:Exome sequencing of Alcohol-associated Hepatitis

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Alcohol-associated hepatitis induces hepatocyte senescence which is reduced following disease resolution

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-28 | GSE270043 | GEO

Host senescence determines the success of hepatocyte transplantation in a mouse model of liver injury

Project description:Hepatocyte transplantation has shown promise for genetic diseases but has mixed efficacy for acute and severe liver injury. Limited cell engraftment and poor function of donor hepatocytes in recipient liver are significant hurdles for clinical efficacy. Hepatocyte senescence is a key feature of many liver diseases. Senescence-driven liver injury could be induced in Ahcre+Mdm2fl/fl mice in controlled and predictable levels through excision of hepatocyte Mdm2. Host senescence and injury was a requirement for initial donor hepatocyte engraftment and repopulation, but too much was inhibitory to this. Long-term expansion of transplanted hepatocytes improved histological features of injury and liver function. However graft function could spontaneously decline due to transmission of senescence from host to donor cells. Modification of the host niche prior to transplantation with senotherapeutic drug ABT737 improved donor cell proliferative capacity. Targeting paracrine senescence may be a way to improve donor hepatocyte function, optimise therapy and guide translation into the clinics.

2025-01-31 | GSE240081 | GEO

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