Evidence map›Paper›PMID 37309415›Full record

ArticleDrug design, development and therapy2023

Exploration of Artemisinin Against IgA Nephropathy via AKT/Nrf2 Pathway by Bioinformatics and Experimental Validation.

Wei-Guang Yang, Ao Sun, Rong Zhu, Nan Liu, Wei-Jie He, Lin-Lin Liu

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  3. Advances in the Targeted Drug Delivery System for Renal Fibrosis.International journal of nanomedicine · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Wei-Guang Yang *Department of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.
Ao Sun *Department of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.ORCID 0009-0007-6615-6613
Rong ZhuDepartment of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.
Nan LiuDepartment of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.
Wei-Jie HeDepartment of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.
Lin-Lin LiuDepartment of Nephrology, The First Affiliated Hospital of China Medical University, Shen Yang, Liao Ning, People's Republic of China.
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Artemisinin (ART) is a safe and effective antimalarial drug. In recent years, antimalarial drugs have demonstrated a good therapeutic efficacy in IgA nephropathy, suggesting that this may become a new treatment option. Purpose: We aimed to evaluate the effect and mechanism of artemisinin in IgA nephropathy. Methods: In this study, CMap database was used to predict the artemisinin therapeutic effect for IgA nephropathy. A network pharmacology approach was applied to explore the unknown mechanism of artemisinin in IgA nephropathy. We used molecular docking to predict the binding affinity of artemisinin with the targets. A mouse model of IgA nephropathy was established to investigate the therapeutic effect of artemisinin on IgA nephropathy. In vitro, the cell counting Kit-8 assay was used to evaluate the cytotoxicity of artemisinin. Flow cytometry and PCR assays were used to detect the effects of artemisinin on oxidative stress and fibrosis in lipopolysaccharide (LPS)-stimulated mesangial cells. Western blot and immunofluorescence were used to detect the expression of pathway proteins. Results: CMap analysis showed artemisinin may reverse the expression levels of differentially expressed genes in IgA nephropathy. Eighty-seven potential targets of artemisinin in the treatment of IgA nephropathy were screened. Among them, 15 hub targets were identified. Enrichment analysis and GSEA analysis indicated that response to reactive oxygen species is the core biological process. AKT1 and EGFR had the highest docking affinity with artemisinin. In vivo, artemisinin could improve renal injury and fibrosis in mice. In vitro, artemisinin attenuated LPS-induced oxidative stress and fibrosis promoted AKT phosphorylation and Nrf2 nuclear translocation. Conclusion: Artemisinin reduced the level of fibrosis and oxidative stress with IgA nephropathy through the AKT/Nrf2 pathway, which provided an alternative treatment for IgAN.

Indexed as

AntimalarialsArtemisininsGlomerulonephritis, IGAAnimalsComputational BiologyLipopolysaccharidesMiceMolecular Docking SimulationNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktAntimalarialsartemisininArtemisininsLipopolysaccharidesNF-E2-Related Factor 2Proto-Oncogene Proteins c-aktAKTartemisininIgA nephropathynetwork pharmacologyNrf2

Identifiers

PMID37309415
PMCPMC10257916
OpenAlexW4379793074

What OpenQuestion holds

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Registered trials

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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.