Evidence map›Paper›PMID 36447569›Full record

ArticleClinical, cosmetic and investigational dermatology2022

Effect of Azelaic Acid on Psoriasis Progression Investigated Based on Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway.

Licui Li, Huixiu Lu, Yanli Zhang, Qian Li, Shaomin Shi, Yaling Liu

Open access · goldAbstract read
In one paragraph

Article in Clinical, cosmetic and investigational dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Pharmacological Management of Psoriasis: Current Landscape and Future Perspectives.Recent advances in inflammation & allergy drug discovery · 2025
    Review
  6. Article
  7. The effect of azelaic acid on AlClActa neuropsychiatrica · 2024
    Article
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.

Licui LiDepartment of Dermatology and Venereology, Hebei Medical University, Shijiazhuang, People's Republic of China.
Huixiu LuDepartment of Dermatology and Venereology, Hebei Medical University, Shijiazhuang, People's Republic of China.
Yanli ZhangDepartment of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Qian LiDepartment of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Shaomin ShiDepartment of Dermatology, The Third Hospital of Hebei Medical University, Shijiazhuang, People's Republic of China.
Yaling LiuDepartment of Dermatology and Venereology, Hebei Medical University, Shijiazhuang, People's Republic of China.ORCID 0000-0003-4321-399X
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To probe into the effect of azelaic acid on psoriasis based on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Methods: Psoriasis gene expression data were downloaded from the GEO database for differential expression analysis to identify differentially expressed genes (DEGs). KEGG and GSEA analyses were performed to identify important signaling pathways that may be involved in psoriasis progression for subsequent validation. Thirty-six C57BL/6 mice aged 8 weeks old were randomly assigned into the blank control group (n = 9), negative control group (n = 9), psoriasis model group (n = 9), and azelaic acid treat group (n = 9). Mice models of psoriasis were prepared with imiquimod (IMQ) in the latter two groups, and azelaic acid ointment was applied in azelaic acid treat group. Then, hematoxylin-eosin (HE) staining was carried out to detect the effect of azelaic acid on the pathological damage of mice models of psoriasis in each group. HaCaT cells cultured in vitro were divided into blank control group, negative control group (addition of azelaic acid), IL-17 group (20 ng/mL) and IL-17+azelaic acid group, with 3 replicates for each group. Immunofluorescence assay and Western blotting were used to detect the protein expression of PI3K/AKT signaling pathway related molecules. Results: KEGG analysis showed that DEGs were significantly enriched in PI3K-AKT signaling pathway. GSEA analysis showed that PI3K and MTOR signaling pathways were up-regulated in psoriasis, while AUTOPHAGY signaling pathway was down-regulated. HE staining showed that azelaic acid could significantly inhibit the local skin injury in mice caused by IMQ-induced psoriasis. Moreover, azelaic acid can inhibit the expression of PI3K/AKT signaling pathway related proteins phosphorylated (p)-PI3K, p-AKT, p-mammalian target of rapamycin (mTOR), vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), angiogenin-1 and hypoxia-inducible factor-1α (HIF-1α). These results imply that azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis. Conclusion: Azelaic acid may inhibit the activation of PI3K/AKT signaling pathway and angiogenesis, thereby improving the symptoms of psoriasis.

Indexed as

angiogenesisazelaic acidPI3K/AKT signaling pathwaypsoriasis

Identifiers

PMID36447569
PMCPMC9701457
OpenAlexW4309702724

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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.