ArticlePloS one2011
Role and mechanism of arsenic in regulating angiogenesis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 76 citations in OpenAlex.
- Protective Effects of Ellagic Acid Against Arsenic-Induced Hepatotoxicity in Male Wistar Rats: Impact of Heme Oxygenase-1 Upregulation.Food science & nutrition · 2025Article
- Heavy metals: toxicity and human health effects.Archives of toxicology · 2025Review
- Article
- Trace metals and organochlorine pesticide residues in imported fishes in Bangladesh and human health risk implications.Environmental science and pollution research international · 2022Article
- Redox sensitive miR-27a/b/Nrf2 signaling in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
- Dysregulation of microRNAs in metal-induced angiogenesis and carcinogenesis.Seminars in cancer biology · 2021Review
- p62 functions as a signal hub in metal carcinogenesis.Seminars in cancer biology · 2021Review
- Paradoxical effects of arsenic in the lungs.Environmental health and preventive medicine · 2021Review
- Inorganic arsenic induces sex-dependent pathological hypertrophy in the heart.American journal of physiology. Heart and circulatory physiology · 2021Article
- Anti-Cancer Agents in Proliferation and Cell Death: The Calcium Connection.International journal of molecular sciences · 2019Review
- A review of arsenic exposure and lung cancer.Toxicology research · 2019Review
- PI3K/Akt/mTOR Signaling Pathway and the Biphasic Effect of Arsenic in Carcinogenesis.Molecular pharmacology · 2018Review
- Nickel induces transcriptional down-regulation of DNA repair pathways in tumorigenic and non-tumorigenic lung cells.Carcinogenesis · 2017Article
- Endothelial cell calpain as a critical modulator of angiogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Differential transcriptional regulation of hypoxia-inducible factor-1α by arsenite under normoxia and hypoxia: involvement of Nrf2.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Mitochondrial metabolites extend lifespan.Aging cell · 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
- Culture conditions profoundly impact phenotype in BEAS-2B, a human pulmonary epithelial model.Journal of applied toxicology : JAT · 2015Article
- Arsenic and nicotine co-exposure lead to some synergistic effects on oxidative stress and apoptotic markers in young rat blood, liver, kidneys and brain.Toxicology reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Arsenic is a wide spread carcinogen associated with several kinds of cancers including skin, lung, bladder, and liver cancers. Lung is one of the major targets of arsenic exposure. Angiogenesis is the pivotal process during carcinogenesis and chronic pulmonary diseases, but the role and mechanism of arsenic in regulating angiogenesis remain to be elucidated. In this study we show that short time exposure of arsenic induces angiogenesis in both human immortalized lung epithelial cells BEAS-2B and adenocarcinoma cells A549. To study the molecular mechanism of arsenic-inducing angiogenesis, we find that arsenic induces reactive oxygen species (ROS) generation, which activates AKT and ERK1/2 signaling pathways and increases the expression of hypoxia-inducible factor 1 (HIF-1) and vascular endothelial growth factor (VEGF). Inhibition of ROS production suppresses angiogenesis by decreasing AKT and ERK activation and HIF-1 expression. Inhibition of ROS, AKT and ERK1/2 signaling pathways is sufficient to attenuate arsenic-inducing angiogenesis. HIF-1 and VEGF are downstream effectors of AKT and ERK1/2 that are required for arsenic-inducing angiogenesis. These results shed light on the mechanism of arsenic in regulating angiogenesis, and are helpful to develop mechanism-based intervention to prevent arsenic-induced carcinogenesis and angiogenesis in the future.
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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.