ArticleLipids in health and disease2015
Fibrinogen production is enhanced in an in-vitro model of non-alcoholic fatty liver disease: an isolated risk factor for cardiovascular events?
Article in Lipids in health and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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.
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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- DNA methylation age is associated with an altered hemostatic profile in a multiethnic meta-analysis.Blood · 2018Pooled it
- The application of artificial intelligence in the intersection of metabolic dysfunction-associated steatotic liver disease and cardiovascular diseases.Frontiers in immunology · 2026Review
- Insights into Non-Alcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis: The Role of Fibrinogen and Pepsinogen.Middle East journal of digestive diseases · 2025Review
- Construction and Evaluation of Neural Network Correlation Model between Syndrome Elements and Physical and Chemical Indexes of Unstable Angina Pectoris Complicated with Anxiety.Computational and mathematical methods in medicine · 2022Article
- Cell Models and Omics Techniques for the Study of Nonalcoholic Fatty Liver Disease: Focusing on Stem Cell-Derived Cell Models.Antioxidants (Basel, Switzerland) · 2021Review
- Non-alcoholic fatty liver disease - a procoagulant condition?Croatian medical journal · 2021Review
- NAFLD and Cardiovascular Diseases: Epidemiological, Mechanistic and Therapeutic Considerations.Journal of clinical medicine · 2021Review
- Fibrinogen Increases Resveratrol Solubility and Prevents it from Oxidation.Foods (Basel, Switzerland) · 2020Article
- hiPSC hepatocyte model demonstrates the role of unfolded protein response and inflammatory networks in αJournal of hepatology · 2018Article
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- Erratum to: Fibrinogen production is enhanced in an in-vitro model of non-alcoholic fatty liver disease: an isolated risk factor for cardiovascular events?Lipids in health and disease · 2016Article
- Proteomic profiling of cellular steatosis with concomitant oxidative stress in vitro.Lipids in health and disease · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCardiovascular disease (CVD) remains the major cause of excess mortality in patients with non-alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the individual contribution of NAFLD to CVD risk factors in the absence of pathogenic influences from other comorbidities often found in NAFLD patients, by using an established in-vitro model of hepatic steatosis.
methodsHistopathological events in non-alcoholic fatty liver disease were recapitulated by focused metabolic nutrient overload of hepatoblastoma C3A cells, using oleate-treated-cells and untreated controls for comparison. Microarray and proteomic data from cell culture experiments were integrated into a custom-built systems biology database and proteogenomics analysis performed. Candidate genes with significant dysregulation and concomitant changes in protein abundance were identified and STRING association and enrichment analysis performed to identify putative pathogenic pathways.
resultsThe search strategy yielded 3 candidate genes that were specifically and significantly up-regulated in nutrient-overloaded cells compared to untreated controls: fibrinogen alpha chain (2.2 fold), fibrinogen beta chain (2.3 fold) and fibrinogen gamma chain (2.1 fold) (all rank products pfp <0.05). Fibrinogen alpha and gamma chain also demonstrated significant concomitant increases in protein abundance (3.8-fold and 2.0-fold, respectively, p <0.05).
conclusionsIn-vitro modelling of NAFLD and reactive oxygen species formation in nutrient overloaded C3A cells, in the absence of pathogenic influences from other comorbidities, suggests that NAFLD is an isolated determinant of CVD. Nutrient overload-induced up-regulation of all three fibrinogen component subunits of the coagulation cascade provides a possible mechanism to explain the excess CVD mortality observed in NAFLD patients.
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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.