ArticleClinical proteomics2025
Comprehensive analysis of chronic hepatitis B concurrent with non-alcoholic fatty liver disease: a proteomics report based on clinical liver samples.
Article in Clinical proteomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Neohesperidin Regulates Lipid Metabolism and Ameliorates MASLD by Targeting ECHS1.Phytotherapy research : PTR · 2026Article
- Article
- MASLD and viral hepatitis overlap: An emerging dual burden in chronic liver disease.Hepatology forum · 2026Review
- Macrophage-linked lipid metabolic signatures for HCC prognosis identified through integrated bulk and single-cell transcriptomics.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
BACKGROUND AND
aimsIn recent years, the prevalence of non-alcoholic fatty liver disease (NAFLD) has risen among patients with chronic hepatitis B (CHB), coinciding with the increasing rates of obesity and metabolic syndrome. Both conditions can contribute to liver fibrosis and even hepatocellular carcinoma; however, the pathogenesis of each disease, as well as CHB concurrent with NAFLD, remains incompletely understood.
methodsWe comprehensively analyzed protein levels in liver tissues from four distinct groups: healthy controls, patients with CHB, patients with NAFLD, and those with CHB and NAFLD using proteomic profiling. Subsequently, we performed bioinformatics analyses based on the results of differentially expressed proteins (DEPs). We also verified the levels of select DEPs in both patient liver samples and a murine model.
resultsOur investigation revealed that enhanced viral clearance in patients with hepatitis B virus (HBV) with concurrent NAFLD might be associated with an inflammatory response and the activation of numerous metabolic pathways within the body. Meanwhile, the degree of hepatic steatosis was associated with anomalies in fatty acid degradation, glycolysis/gluconeogenesis, and other metabolic processes. However, the prognosis for patients with CHB and concurrent NAFLD may be severe, and this may be connected to the altered levels of proteins such as ACAT1, ACY1, SERPINB3, MTCH2, ALDH2, ECHS1, S100A7, and LRP6.
conclusionIn comparison to CHB and NAFLD alone, the prognosis for CHB complicated by NAFLD appears less favorable. This disparity is closely correlated with distinct protein level patterns in the liver following the onset of both diseases. Our study provides novel insights into the disease progression and clinical mechanisms underlying CHB and NAFLD.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.