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Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

ABSTRACT: Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

PROVIDER: PRJNA580468 | ENA |

REPOSITORIES: ENA

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Molecular characterization of chronic liver disease dynamics: from liver fibrosis to acute-on-chronic liver failure

Project description:BACKGROUND: The molecular mechanisms driving the progression from early chronic liver disease (eCLD) to cirrhosis and, finally, acute-on-chronic liver failure (ACLF) are largely unknown. Thus, the aim of this work is to develop a network-based approach to investigate molecular pathways driving progression from eCLD to ACLF. We created 9 liver-specific biological networks capturing key pathophysiological processes potentially related to CLD. We used these networks as framework to perform gene set enrichment analyses(GSEA) and create dynamic profiles of disease progression. RESULTS: Principal component analyses revealed that samples clustered according to the disease stage. GSEA analyses of the defined processes showed an up-regulation of inflammation, fibrosis and apoptosis networks throughout disease progression. Interestingly, we did not find significant gene expression differences between CC and DC, while ACLF showed acute expression changes in all the defined liver-related networks. The analyses of disease progression patterns identified ascending and descending expression profiles associated to ACLF onset. Functional analyses showed that ascending profiles were associated to inflammation, fibrosis, apoptosis, senescence and carcinogenesis networks, while descending profiles were mainly related to oxidative stress and genetic factors. We confirmed by qPCR the up-regulation of 4 genes of the ascending profile CXCL-6, KRT-18, SPINK-1, and ITGA2, and validated our findings on an independent patient’s cohort. CONCLUSION: ACLF is characterized by a specific hepatic gene expression pattern related to inflammation, fibrosis, apoptosis, senescence and carcinogenesis processes. Moreover, the observed profile is significantly different from that of compensated and decompensated cirrhosis, supporting thus the hypothesis that ACLF should be considered a distinct entity.

2021-09-11 | GSE139602 | GEO

Transcriptomic Characterization of Liver Tissue Changes in Human and Mice with Acute-on-Chronic Liver Failure and Liver Cirrhosis/Fibrosis

Project description:This study aims to investigate gene expression differences at the transcriptional level in liver tissue from acute-on-chronic liver failure (ACLF) compared to liver cirrhosis (CLD, human) or Fibrosis (mice) and healthy control groups.For human samples, they were categorized into ACLF, CLD, and healthy control (HC) groups. For mouse samples, they were divided into ACLF, Fibrosis, and HC groups.

2026-02-13 | GSE298435 | GEO

Transcriptomic Characterization of Liver Tissue Changes in Human and Mice with Acute-on-Chronic Liver Failure and Liver Cirrhosis/Fibrosis

Project description:Transcriptomic Characterization of Liver Tissue Changes in Human and Mice with Acute-on-Chronic Liver Failure and Liver Cirrhosis/Fibrosis

| PRJNA1269436 | ENA

Serum EV proteome target analysis of liver fibrosis in chronic hepatitis C patients

Project description:Serum EV proteome target analysis of liver fibrosis in chronic hepatitis C patients was performed.

2023-01-27 | PXD031289 | JPOST Repository

Serum EV proteome non-target analysis of liver fibrosis in chronic hepatitis C patients

Project description:Serum EV proteome non-target analysis of liver fibrosis in chronic hepatitis C patients was performed using TMT-tag quantitation.

2023-01-26 | PXD031283 | JPOST Repository

The role of Angiopoietin 1 in acute-on-chronic liver failure

Project description:Acute-on-chronic liver failure (ACLF) is an acute liver and multisystem failure in patients with pre-existing liver disease. A common precipitating factor for ACLF is sepsis. Our recent work shows that sepsis-ACLF is associated with loss of Angiopoietin 1 (ANG-1) and endothelial dysfunction that in turn promotes loss of hepatocyte differentiation and liver failure. However, the mechanism of angiopoietin-mediated endothelial to hepatocyte crosstalk in ACLF is not fully understood. We aimed to study Angiopoietin 1-induced changes in liver cells using spatial transcritomics.

2026-09-01 | GSE342343 | GEO

Molecular characterization of chronic liver disease dynamics: From liver fibrosis to acute-on-chronic liver failure.

Project description: Not available

| S-EPMC9079303 | biostudies-literature

Liver fibrosis

Project description:Liver fibrosis

| PRJNA857444 | ENA

development of prognostic biomarkers for HBV-related acute-on-chronic liver failure

Project description:development of prognostic biomarkers for HBV-related acute-on-chronic liver failure

2020-03-07 | PXD017928 |

Macrophage-Derived CXCR4 Accelerates the Progression of Acute-on-chronic Liver Failure by Promoting Liver Fibrosis and Inflammation via the TGF-β/SMAD and MAPK Pathways

Project description:Acute-on-chronic liver failure (ACLF) is a severe syndrome characterized by intense inflammation and fibrosis, yet effective targeted therapies remain limited. This study aimed to elucidate the functional role and underlying mechanism of C-X-C chemokine receptor type 4 (CXCR4) in ACLF pathogenesis. Using an integrated multiomics approach encompassing transcriptomic reanalysis, clinical validation, and single-cell RNA sequencing (scRNA-seq) of livers from a murine ACLF model, we identified a Cxcr4+ macrophage subpopulation that served as a central communication hub. In vivo gain- and loss-of-function studies demonstrated that AAV-mediated macrophage-specific CXCR4 overexpression exacerbated liver injury, inflammation, fibrosis, and mortality, whereas pharmacological inhibition with AMD3100 conferred significant protection. Mechanistically, transcriptomic and biochemical analyses revealed that CXCR4 coordinately hyperactivated the TGF-β/SMAD and MAPK signaling networks. In vitro coculture assays further confirmed that genetic knockdown of Cxcr4 in macrophages abolished their capacity to activate hepatic stellate cells. Collectively, these findings establish macrophage-derived CXCR4 as a critical promoter of ACLF progression that synchronizes inflammation and fibrosis through the TGF-β/SMAD and MAPK pathways, positioning CXCR4 as a promising therapeutic target for this devastating syndrome.

2026-09-15 | GSE346778 | GEO

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