ArticleBiological trace element research2023
Signaling Pathways and Genes Associated with Hexavalent Chromium-Induced Hepatotoxicity.
Article in Biological trace element research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Understanding and using Animal Models of Hepatotoxicity.Current pharmaceutical design · 2025Review
- Study on the metabolic effects of hexavalent chromium [Cr (VI)] on rat astrocytes using un-targeted metabolomics.Frontiers in molecular biosciences · 2024Article
- Revisiting the potential of regulated cell death in glioma treatment: a focus on autophagy-dependent cell death, anoikis, ferroptosis, cuproptosis, pyroptosis, immunogenic cell death, and the crosstalk between them.Frontiers in oncology · 2024Review
- Hexavalent-Chromium-Induced Oxidative Stress and the Protective Role of Antioxidants against Cellular Toxicity.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Exposure to hexavalent chromium [Cr(VI)] causes human and animal hepatotoxicity. However, it is unclear how Cr(VI) induces hepatotoxicity, nor is it clear which pathways and genes may be involved. This study aimed to identify the key molecular pathways and genes engaged in Cr(VI)-induced hepatotoxicity. Publicly available microarray GSE19662 was downloaded from the Gene Expression Omnibus database. GSE19662 consists of primary rat hepatocyte (PRH) groups treated with or without 0.10 ppm potassium dichromate (PD), with three samples per group. Compared to the control group, a total of 400 differentially expressed genes were obtained. Specially 262 and 138 genes were up- and downregulated in PD-treated PRHs, respectively. Gene ontology (GO) enrichment indicated that those DEGs were primarily engaged in many biological processes, including androgen biosynthetic process, the positive regulation of cell death, the response to activity, the toxic substance and hepatocyte growth factor stimulus, and others. Kyoto Encyclopedia of Genes and Genomes (KEGG) suggested that the DEGs are fundamentally enriched in hepatocellular carcinoma (HCC), hepatitis B, p53, PI3K-Akt, MAPK, AMPK, metabolic pathways, estrogen, cGMP-PKG, metabolic pathways, etc. Moreover, many genes, including UBE2C, TOP2A, PRC1, CENPF, and MKI67, might contribute to Cr(VI)-induced hepatotoxicity. Taken together, this study enhances our understanding of the regulation, prevention, and treatment strategies of Cr(VI)-induced hepatotoxicity.
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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.