ReviewCell death & disease2025
ACBP/DBI neutralization for the prevention and treatment of malignant and non-malignant liver diseases.
Review in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Acyl coenzyme A binding protein (ACBP), also known as diazepam binding inhibitor (DBI), suppresses autophagy, stimulates food intake, and regulates body composition. This tissue hormone contributes to the development of age-related diseases such as metabolic syndrome, cardiovascular disease, cancer, and osteoarthritis. ACBP/DBI also plays a key pathogenic role in liver disorders, including hepatocellular carcinoma (HCC). Circulating levels of ACBP/DBI are elevated in patients with histologically diagnosed steatosis, liver fibrosis or HCC, and correlate with disease severity. Moreover, the incidence of liver cancers increases in individuals receiving benzodiazepines, which act on the same binding sites of the GABA-A receptor as ACBP/DBI. In mice, inhibiting ACBP/DBI, via inducible knockout, mutation of its receptor (the γ2 subunit of the GABA-A receptor) or antibody-mediated neutralization, alleviates various liver conditions, including ischemia-reperfusion injury, bile duct obstruction, hepatotoxicity of acetaminophen, CCl
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