ArticleFrontiers in molecular biosciences2021
LECT2, A Novel and Direct Biomarker of Liver Fibrosis in Patients With CHB.
Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- ITPR3 promotes liver fibrosis by damaging hepatocytes via the Ca2+/NF-B/LECT2 pathway.Scientific reports · 2026Article
- The Role of Organokines in Obesity and Type 2 Diabetes and Their Functions as Molecular Transducers of Nutrition and Exercise.Metabolites · 2023Review
- Will inhibition of cellular crosstalk resolve liver fibrosis?Hepatology (Baltimore, Md.) · 2022Article
- LECT2: A pleiotropic and promising hepatokine, from bench to bedside.Journal of cellular and molecular medicine · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B (CHB) patients with severe liver fibrosis would be more likely to progress to a poorer prognosis. Treatment is considered once the liver fibrosis reaches significant liver fibrosis (≥S2). Leukocyte cell-derived chemotaxin-2 (LECT2) has been shown to contribute to liver fibrosis progression. No research has focused on the role of LECT2 in liver fibrosis in CHB patients. This study enrolled 227 CHB patients and divided them into the training group (
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Registered trials
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