ArticleToxicology and applied pharmacology2007
Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice.
Article in Toxicology and applied pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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
29 citing papers in PubMed, 71 citations in OpenAlex.
- 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
- 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
- Heavy metal pollution and ischemic stroke: multimechanistic pathogenesis and countermeasures.Frontiers in public health · 2025Review
- Mechanisms of Metal-Induced Hepatic Inflammation.Current environmental health reports · 2024Review
- Article
- Arsenic exposure from drinking water and endothelial dysfunction in Bangladeshi adolescents.Environmental research · 2022Article
- Targeting Liver Sinusoidal Endothelial Cells: An Attractive Therapeutic Strategy to Control Inflammation in Nonalcoholic Fatty Liver Disease.Frontiers in pharmacology · 2021Review
- Arsenic Directs Stem Cell Fate by Imparting Notch Signaling Into the Extracellular Matrix Niche.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Lipid and Cholesterol Homeostasis after Arsenic Exposure and Antibiotic Treatment in Mice: Potential Role of the Microbiota.Environmental health perspectives · 2019Article
- Urine Arsenic and Arsenic Metabolites in U.S. Adults and Biomarkers of Inflammation, Oxidative Stress, and Endothelial Dysfunction: A Cross-Sectional Study.Environmental health perspectives · 2017Article
- Evaluation of vascular effect of arsenic using in vivo assays.Environmental science and pollution research international · 2017Article
- Chronic early childhood exposure to arsenic is associated with a TNF-mediated proteomic signaling response.Environmental toxicology and pharmacology · 2017Article
- A cross sectional study of anemia and iron deficiency as risk factors for arsenic-induced skin lesions in Bangladeshi women.BMC public health · 2016Article
- Functional role of inorganic trace elements in angiogenesis part III: (Ti, Li, Ce, As, Hg, Va, Nb and Pb).Critical reviews in oncology/hematology · 2016Review
- Identification of Id1 as a downstream effector for arsenic-promoted angiogenesisToxicology research · 2016Article
- Arsenic induces structural and compositional colonic microbiome change and promotes host nitrogen and amino acid metabolism.Toxicology and applied pharmacology · 2015Article
- Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis.Carcinogenesis · 2015Review
- Mathematical model of blood and interstitial flow and lymph production in the liver.Biomechanics and modeling in mechanobiology · 2014Article
- In utero and early life arsenic exposure in relation to long-term health and disease.Toxicology and applied pharmacology · 2013Review
- Preliminary morphological and biochemical changes in rat liver following postnatal exposure to sodium arsenite.Anatomy & cell biology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The vascular effects of arsenic in drinking water are global health concerns contributing to human disease worldwide. Arsenic targets the endothelial cells lining blood vessels, and endothelial cell activation or dysfunction may underlie the pathogenesis of both arsenic-induced vascular diseases and arsenic-enhanced tumorigenesis. The purpose of the current studies was to demonstrate that exposing mice to drinking water containing environmentally relevant levels of arsenic promoted endothelial cell dysfunction and pathologic vascular remodeling. Increased angiogenesis, neovascularization, and inflammatory cell infiltration were observed in Matrigel plugs implanted in C57BL/6 mice following 5-week exposures to 5-500 ppb arsenic [Soucy, N.V., Mayka, D., Klei, L.R., Nemec, A.A., Bauer, J.A., Barchowsky, A., 2005. Neovascularization and angiogenic gene expression following chronic arsenic exposure in mice. Cardiovasc.Toxicol 5, 29-42]. Therefore, functional in vivo effects of arsenic on endothelial cell function and vessel remodeling in an endogenous vascular bed were investigated in the liver. Liver sinusoidal endothelial cells (LSEC) became progressively defenestrated and underwent capillarization to decrease vessel porosity following exposure to 250 ppb arsenic for 2 weeks. Sinusoidal expression of PECAM-1 and laminin-1 proteins, a hallmark of capillarization, was also increased by 2 weeks of exposure. LSEC caveolin-1 protein and caveolae expression were induced after 2 weeks of exposure indicating a compensatory change. Likewise, CD45/CD68-positive inflammatory cells did not accumulate in the livers until after LSEC porosity was decreased, indicating that inflammation is a consequence and not a cause of the arsenic-induced LSEC phenotype. The data demonstrate that the liver vasculature is an early target of pathogenic arsenic effects and that the mouse liver vasculature is a sensitive model for investigating vascular health effects of arsenic.
Indexed as
Identifiers
What OpenQuestion holds
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.