Evidence map›Paper›PMID 37999215›Full record

ArticleMetabolites2023

Fibroblast Growth Factor 21 in Chronic Hepatitis C: A Potential Non-Invasive Biomarker of Liver Status upon Viral Eradication.

Filippo Biagi, Francesco Carlomagno, Martina Carbone, Roberta Veralli, Umberto Vespasiani-Gentilucci, Elisabetta Riva, Silvia Manfrini, Dario Tuccinardi, Adriano De Santis, Lucio Gnessi and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Metabolites, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 40% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 1 country.

Filippo BiagiDepartment of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy.
Francesco CarlomagnoDepartment of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy.ORCID 0000-0001-5611-4101
Martina CarboneDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00185 Rome, Italy.
Roberta VeralliClinical Laboratory Unit, Fondazione Policlinico Universitario Campus Bio-Medico, 00128 Rome, Italy.ORCID 0000-0002-9646-1375
Umberto Vespasiani-GentilucciUnit of Clinical Medicine and Hepatology, Area of Medicine, Campus Bio-Medico University of Rome, 00128 Rome, Italy.
Elisabetta RivaUnit of Virology, Fondazione Policlinico Universitario Campus Bio-Medico, 00128 Rome, Italy.
Silvia ManfriniDepartment of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, 00128 Rome, Italy.
Dario TuccinardiDepartment of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, 00128 Rome, Italy.
Adriano De SantisDepartment of Translational and Precision Medicine, Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0001-7338-9203
Lucio GnessiDepartment of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy.
Mikiko WatanabeDepartment of Experimental Medicine, Section of Medical Pathophysiology, Food Science and Endocrinology, Sapienza University of Rome, 00161 Rome, Italy.ORCID 0000-0003-2225-8814
Sapienza University of Rome · ITUniversità Campus Bio-Medico · ITCampus Bio Medico University Hospital · ITOspedale Santa Maria della Misericordia di Udine · ITUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast growth factor 21 (FGF-21), previously recognized as a marker of liver damage and a potential drug target in non-alcoholic fatty liver disease (NAFLD), has unclear implications in hepatitis C virus (HCV) infections. This study aimed to investigate the relationship between FGF-21 levels and liver health in patients with HCV undergoing direct-acting antiviral (DAA) treatment. Forty-five patients were assessed for liver stiffness, blood chemistry, and other relevant metrics before and after achieving sustained viral response (SVR), defined as the absence of detectable HCV-RNA after 24 weeks of treatment. Post-treatment, all patients showed a decrease in liver stiffness and improved liver enzyme levels (AST and ALT), alongside an increase in FGF-21 levels. Interestingly, the increase in FGF-21 correlated negatively with liver stiffness but showed no correlation with hepatic steatosis. The observed elevation in FGF-21 levels at SVR following DAA therapy for chronic HCV infection can be attributed to the restoration of hepatic function, including its synthetic capabilities. Specifically, the mitigation of liver fibrosis post-HCV eradication is expected to lead to improvements in liver function, such as enhanced albumin and FGF-21 production. This improvement in synthetic function likely drives the increase in FGF-21 levels, rather than changes in liver fat content. We suggest a potential role of FGF-21 as a marker of fibrosis and hepatic cytotoxicity and as a drug target beyond NAFLD, to be confirmed by additional studies.

Indexed as

cirrhosisDAAsFGF-21HCVNAFLDNASH

Identifiers

PMID37999215
PMCPMC10673401
OpenAlexW4388017582

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.