ArticleWorld journal of gastroenterology2024
Mitochondrial dysfunction affects hepatic immune and metabolic remodeling in patients with hepatitis B virus-related acute-on-chronic liver failure.
Article in World journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Agrimoniin ameliorates intrapulmonary angiogenesis and improves hypoxemia in hepatopulmonary syndrome via PGC-1α activation and glycolysis down-regulation.Genes & diseases · 2026Article
- Altered TAGLN Expression During HBV Replication Correlates with OPA1 Levels.International journal of molecular sciences · 2026Article
- Characterization of multi-stage metabolic alterations in hepatitis B virus-related acute-on-chronic liver failure using high-coverage metabolomics.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- The pivotal role of mitochondria in the pathogenesis and treatment of liver failure: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Study on the effect of Portulaca oleracea L. extract on chronic ulcerative colitis in rats induced by allogeneic antigen and acetic acid.Acta cirurgica brasileira · 2026Article
- Single-Cell Analysis of Hepatic Non-Parenchymal Cells Reveals Endothelial Dysfunction and Altered Endothelial and B Cell Communication in Acute-on-Chronic Liver Failure.Journal of immunology research · 2026Article
- Growth differentiation factor-15 as a non-invasive biomarker of liver fibrosis in sickle cell disease.International journal of hematology · 2025Article
- Role of cellular senescence in hepatic diseases (Review).International journal of molecular medicine · 2025Review
- Immunological Mechanisms and Effects of Bacterial Infections in Acute-on-Chronic Liver Failure.Cells · 2025Review
- High glycosylated serum protein to high density lipoprotein cholesterol ratios are predictive of worse acute on chronic liver failure prognoses.Scientific reports · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune dysregulation and metabolic derangement have been recognized as key factors that contribute to the progression of hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF). However, the mechanisms underlying immune and metabolic derangement in patients with advanced HBV-ACLF are unclear.
aimTo identify the bioenergetic alterations in the liver of patients with HBV-ACLF causing hepatic immune dysregulation and metabolic disorders.
methodsLiver samples were collected from 16 healthy donors (HDs) and 17 advanced HBV-ACLF patients who were eligible for liver transplantation. The mitochondrial ultrastructure, metabolic characteristics, and immune microenvironment of the liver were assessed. More focus was given to organic acid metabolism as well as the function and subpopulations of macrophages in patients with HBV-ACLF.
resultsCompared with HDs, there was extensive hepatocyte necrosis, immune cell infiltration, and ductular reaction in patients with ACLF. In patients, the liver suffered severe hypoxia, as evidenced by increased expression of hypoxia-inducible factor-1α. Swollen mitochondria and cristae were observed in the liver of patients. The number, length, width, and area of mitochondria were adaptively increased in hepatocytes. Targeted metabolomics analysis revealed that mitochondrial oxidative phosphorylation decreased, while anaerobic glycolysis was enhanced in patients with HBV-ACLF. These findings suggested that, to a greater extent, hepa-tocytes used the extra-mitochondrial glycolytic pathway as an energy source. Patients with HBV-ACLF had elevated levels of chemokine C-C motif ligand 2 in the liver homogenate, which stimulates peripheral monocyte infiltration into the liver. Characterization and functional analysis of macrophage subsets revealed that patients with ACLF had a high abundance of CD68
conclusionThe results indicated that bioenergetic alteration driven by hypoxia and mitochondrial dysfunction affects hepatic immune and metabolic remodeling, leading to advanced HBV-ACLF. These findings highlight a new therapeutic target for improving the treatment of HBV-ACLF.
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