Evidence map›Paper›PMID 38469298›Full record

ArticleFrontiers in immunology2024

Histidine-rich glycoprotein in metabolic dysfunction-associated steatohepatitis-related disease progression and liver carcinogenesis.

Beatrice Foglia, Salvatore Sutti, Stefania Cannito, Chiara Rosso, Marina Maggiora, Alice Casalino, Claudia Bocca, Erica Novo, Francesca Protopapa, Naresh Naik Ramavath and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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  8. Cysteine-rich 61 inhibition attenuates hepatic insulin resistance and improves lipid metabolism in high-fat diet fed mice and HepG2 cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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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

16 authors at 4 institutions in 3 countries.

Beatrice Foglia *Department Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Salvatore Sutti *Department Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of Eastern Piedmont, Novara, Italy.
Stefania CannitoDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Chiara RossoDepartment Medical Sciences, University of Torino, and Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.
Marina MaggioraDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Alice CasalinoDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Claudia BoccaDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Erica NovoDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Francesca ProtopapaDepartment Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
Naresh Naik RamavathDepartment of Pediatrics, School of Medicine, Washington University, St Louis, MO, United States.
Alessia ProveraDepartment Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of Eastern Piedmont, Novara, Italy.
Alessandro GambellaDepartment Medical Sciences, University of Torino, and Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.
Elisabetta BugianesiDepartment Medical Sciences, University of Torino, and Division of Gastroenterology, San Giovanni Hospital, Torino, Italy.
Frank TackeDepartment of Hepatology and Gastroenterology, Charité-Universitatsmedizin Berlin, Berlin, Germany.
Emanuele Albano *Department Health Sciences and Interdisciplinary Research Centre for Autoimmune Diseases, University Amedeo Avogadro of Eastern Piedmont, Novara, Italy.
Maurizio Parola *Department Clinical and Biological Sciences, Unit of Experimental Medicine and Clinical Pathology, University of Torino, Torino, Italy.
University of Turin · ITUniversità degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITCharité - Universitätsmedizin Berlin · DEWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD), previously non-alcoholic fatty liver disease (NAFLD), is a leading cause of chronic liver disease worldwide. In 20%-30% of MASLD patients, the disease progresses to metabolic dysfunction-associated steatohepatitis (MASH, previously NASH) which can lead to fibrosis/cirrhosis, liver failure as well as hepatocellular carcinoma (HCC). Here we investigated the role of histidine-rich glycoprotein (HRG), a plasma protein produced by hepatocytes, in MASLD/MASH progression and HCC development. Methods: The role of HRG was investigated by morphological, cellular, and molecular biology approaches in (a) HRG Results: In non-neoplastic settings, murine and clinical data indicate that HRG increases significantly in parallel with disease progression. In particular, in MASLD/MASH patients, higher levels of HRG plasma levels were detected in subjects with extensive fibrosis/cirrhosis. When submitted to the pro-carcinogenic protocol, HRG Conclusion: Murine and clinical data indicate that HRG plays a significant role in MASLD/MASH progression to HCC by supporting a specific population of tumor-associated macrophages with pro-inflammatory response and pro-angiogenetic capabilities which critically support cancer cell survival. Furthermore, our data suggest HRG as a possible prognostic predictor in HCC patients with MASLD/MASH-related HCCs.

Indexed as

AcetamidesCarcinoma, HepatocellularLiver NeoplasmsMetabolic DiseasesNon-alcoholic Fatty Liver DiseaseProteinsAnimalsCarcinogenesisDisease ProgressionHistidine-Rich GlycoproteinHumansLiver CirrhosisMiceAcetamidesCDAAHistidine-Rich GlycoproteinProteinschronic liver diseasesfibrogenesisHCChepatocellular carcinomahistidine-rich glycoproteininflammationliver carcinogenesisMASH

Identifiers

PMID38469298
PMCPMC10925642
OpenAlexW4392167170

What Socratic holds

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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 Socratic graph.