Trial reportThe Journal of clinical investigation2015
Vascular adhesion protein-1 promotes liver inflammation and drives hepatic fibrosis.
Trial report in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
129 citing papers in PubMed, 209 citations in OpenAlex.
- Proof-of-concept PET imaging of pulmonary sarcoidosis using VAP-1-targeted radiotracer [Respiratory research · 2025Trial
- Vascular adhesion protein-1 blockade in primary sclerosing cholangitis: Open-label, multicenter, single-arm, phase II trial.Hepatology communications · 2024Trial
- A randomised Phase IIa trial of amine oxidase copper-containing 3 (AOC3) inhibitor BI 1467335 in adults with non-alcoholic steatohepatitis.Nature communications · 2023Trial
- Senescent Human Liver Endothelial Cells Mediate CD4Immunology · 2026Article
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
- Hepatocyte-hepatic stellate cell interactions in liver fibrosis: Mechanisms and therapeutic implications.Hepatology communications · 2026Review
- The "Immune Rebellion" from the Intestines to the Liver: A Vicious Cycle That Causes the Liver to Collapse.Metabolites · 2026Review
- Targeted degradation of GSPT1 and NEK7 by a molecular glue prodrug for treatment of HCC.Communications chemistry · 2025Article
- MASLD development: From molecular pathogenesis toward therapeutic strategies.Chinese medical journal · 2025Review
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- The role of liver sinusoidal endothelial cells in metabolic dysfunction-associated steatotic liver diseases and liver cancer: mechanisms and potential therapies.Angiogenesis · 2025Review
- Interaction between mitochondrial oxidative stress and myocardial fibrosis in the context of diabetes.Frontiers in endocrinology · 2025Review
- Mechanism-guided drug development and treatment for liver fibrosis: a clinical perspective.Frontiers in pharmacology · 2025Review
- The role of VAP-1 in cardiovascular disease: a review.Frontiers in cardiovascular medicine · 2025Review
- The microenvironment in the development of MASLD-MASH-HCC and associated therapeutic in MASH-HCC.Frontiers in immunology · 2025Review
- Examination of the causal role of immune cells in non-alcoholic fatty liver disease by a bidirectional Mendelian randomization study.Open medicine (Warsaw, Poland) · 2025Article
- The role of vascular adhesion protein-1 in diabetes and diabetic complications.Journal of diabetes investigation · 2024Review
- Depletion of Activated Hepatic Stellate Cells and Capillarized Liver Sinusoidal Endothelial Cells Using a Rationally Designed Protein for Nonalcoholic Steatohepatitis and Alcoholic Hepatitis Treatment.International journal of molecular sciences · 2024Article
- Ovarian fibrosis: molecular mechanisms and potential therapeutic targets.Journal of ovarian research · 2024Review
- Serum Vascular Adhesion Protein-1 and Endothelial Dysfunction in Hepatic Cirrhosis: Searching for New Prognostic Markers.International journal of molecular sciences · 2024Article
69 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses a range of manifestations, including steatosis and cirrhosis. Progressive disease is characterized by hepatic leukocyte accumulation in the form of steatohepatitis. The adhesion molecule vascular adhesion protein-1 (VAP-1) is a membrane-bound amine oxidase that promotes leukocyte recruitment to the liver, and the soluble form (sVAP-1) accounts for most circulating monoamine oxidase activity, has insulin-like effects, and can initiate oxidative stress. Here, we determined that hepatic VAP-1 expression is increased in patients with chronic liver disease and that serum sVAP-1 levels are elevated in patients with NAFLD compared with those in control individuals. In 4 murine hepatic injury models, an absence or blockade of functional VAP-1 reduced inflammatory cell recruitment to the liver and attenuated fibrosis. Moreover, disease was reduced in animals expressing a catalytically inactive form of VAP-1, implicating enzyme activity in the disease pathogenesis. Within the liver, hepatic stromal cells expressed functional VAP-1, and evaluation of cultured cells revealed that sVAP-1 promotes leukocyte migration through catalytic generation of ROS, which depended on VAP-1 enzyme activity. VAP-1 enhanced stromal cell spreading and wound closure and modulated expression of profibrotic genes. Together, these results link the amine oxidase activity of VAP-1 with hepatic inflammation and fibrosis and suggest that targeting VAP-1 has therapeutic potential for NAFLD and other chronic fibrotic liver diseases.
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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.