ArticleHepatology (Baltimore, Md.)2007
Arsenic stimulates sinusoidal endothelial cell capillarization and vessel remodeling in mouse liver.
Article in Hepatology (Baltimore, Md.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Non-cirrhotic portal fibrosis/idiopathic portal hypertension: APASL recommendations for diagnosis and management.Hepatology international · 2024Guideline
- Hepatic inflammation after exposure to a mixture of low-dose arsenic and cadmium in a murine model of fatty liver disease.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Effects of curcumol on ferroptosis and tube forming ability of hepatic sinus endothelial cells.Open medicine (Warsaw, Poland) · 2026Article
- Kupffer cells are essential for platelet-mediated thrombopoietin generation in the liver.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanisms of Metal-Induced Hepatic Inflammation.Current environmental health reports · 2024Review
- Multiple roles of arsenic compounds in phase separation and membraneless organelles formation determine their therapeutic efficacy in tumors.Journal of pharmaceutical analysis · 2024Review
- Baicalein Alleviates Arsenic-induced Oxidative Stress through Activation of the Keap1/Nrf2 Signalling Pathway in Normal Human Liver Cells.Current molecular medicine · 2024Article
- How single-cell transcriptomics provides insight on hepatic responses to TCDD.Current opinion in toxicology · 2023Article
- Review
- Environmental Toxicants and NAFLD: A Neglected yet Significant Relationship.Digestive diseases and sciences · 2022Review
- The roles and mechanisms of hypoxia in liver fibrosis.Journal of translational medicine · 2021Review
- CTRP13 attenuates the expression of LN and CAV-1 Induced by high glucose via CaMKKβ/AMPK pathway in rLSECs.Aging · 2020Article
- Macrophage galactose lectin is critical for Kupffer cells to clear aged platelets.The Journal of experimental medicine · 2020Article
- Review
- Quantitative proteomic study of arsenic treated mouse liver sinusoidal endothelial cells using a reverse super-SILAC method.Biochemical and biophysical research communications · 2019Article
- LSEC Fenestrae Are Preserved Despite Pro-inflammatory Phenotype of Liver Sinusoidal Endothelial Cells in Mice on High Fat Diet.Frontiers in physiology · 2019Article
- Targeting Endothelial Erk1/2-Akt Axis as a Regeneration Strategy to Bypass Fibrosis during Chronic Liver Injury in Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Arsenic exposure and risk of nonalcoholic fatty liver disease (NAFLD) among U.S. adolescents and adults: an association modified by race/ethnicity, NHANES 2005-2014.Environmental health : a global access science source · 2018Article
- Proteomic Analysis Reveals Dab2 Mediated Receptor Endocytosis Promotes Liver Sinusoidal Endothelial Cell Dedifferentiation.Scientific reports · 2017Article
- Anti-angiogenic effect of arsenic trioxide in lung cancer via inhibition of endothelial cell migration, proliferation and tube formation.Oncology letters · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
unlabelledTrivalent arsenic [As(III)] is a well-known environmental toxicant that causes a wide range of organ-specific diseases and cancers. In the human liver, As(III) promotes vascular remodeling, portal fibrosis, and hypertension, but the pathogenesis of these As(III)-induced vascular changes is unknown. To investigate the hypothesis that As(III) targets the hepatic endothelium to initiate pathogenic change, mice were exposed to 0 or 250 parts per billion (ppb) of As(III) in their drinking water for 5 weeks. Arsenic(III) exposure did not affect the overall health of the animals, the general structure of the liver, or hepatocyte morphology. There was no change in the total tissue arsenic levels, indicating that arsenic does not accumulate in the liver at this level of exposure. However, there was significant vascular remodeling with increased sinusoidal endothelial cell (SEC) capillarization, vascularization of the peribiliary vascular plexus (PBVP), and constriction of hepatic arterioles in As(III)-exposed mice. In addition to ultrastructural demonstration of SEC defenestration and capillarization, quantitative immunofluorescence analysis revealed increased sinusoidal PECAM-1 and laminin-1 protein expression, suggesting gain of adherens junctions and a basement membrane. Conversion of SECs to a capillarized, dedifferentiated endothelium was confirmed at the cellular level with demonstration of increased caveolin-1 expression and SEC caveolae, as well as increased membrane-bound Rac1-GTPase.
conclusionThese data demonstrate that exposure to As(III) causes functional changes in SEC signaling for sinusoidal capillarization that may be initial events in pathogenic changes in the liver.
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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.