ArticleOncotarget2016
Bioinformatics facilitating the use of microarrays to delineate potential miRNA biomarkers in aristolochic acid nephropathy.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- TNF-α-induced miR-450a mediates TMEM182 expression to promote oral squamous cell carcinoma motility.PloS one · 2019Article
- Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms.Frontiers in pharmacology · 2019Review
- Investigation into the underlying molecular mechanisms of hypertensive nephrosclerosis using bioinformatics analyses.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aristolochic acid nephropathy (AAN) is a rapidly progressive acute or chronic tubulointerstitial nephritis (TIN). The present study attempted to explore the molecular mechanisms underlying the miRNA-directed development of AAN. Our differentially expressed analysis identified 11 DE-miRNAs and retrieved the target genes of these DE-miRNAs; then, network analysis and functional analysis further identified 6 DE-miRNAs (has-miR-192, has-miR-194, has-miR-542-3p, has-miR-450a, has-miR-584, has-miR-33a) as phenotypic biomarkers of AAN. Surprisingly, of has-miR-192 has been reported to be associated with the pathogenesis of AAN, and has-miR-194, has-miR-542-3p and has-miR-450a was first-time identified to link to the development of AAN. In addition, the expressional changes of has-miR-584 and has-miR-33a may be associated with the development of AAN as well, which must be further confirmed by the associated experiments. Taken together, our work reveals for the first time the regulatory mechanisms of miRNAs in the development of AAN and this will contribute to miRNA-based diagnosis and treatment of AAN.
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Registered trials
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