ArticleBioengineered2022
Dihydroartemisinin targets fibroblast growth factor receptor 1 (FGFR1) to inhibit interleukin 17A (IL-17A)-induced hyperproliferation and inflammation of keratinocytes.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
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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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Mass Spectrometry-Based Proteomics Analysis Unveils PTPRS Inhibits Proliferation and Inflammatory Response of Keratinocytes in Psoriasis.Inflammation · 2025Article
- Advances in the study of artemisinin and its derivatives for the treatment of rheumatic skeletal disorders, autoimmune inflammatory diseases, and autoimmune disorders: a comprehensive review.Frontiers in immunology · 2024Review
- Effects of natural products on skin inflammation caused by abnormal hormones secreted by the adrenal gland.Frontiers in pharmacology · 2023Review
- Transcriptome Analysis Identifies Biomarkers for the Diagnosis and Management of Psoriasis Complicated with Depression.Clinical, cosmetic and investigational dermatology · 2023Article
- miR-124-3p Delivered Using Exosomes Attenuates the Keratinocyte Response to IL-17A Stimulation in Psoriasis.Oxidative medicine and cellular longevity · 2022Article
- Co-expression of fibrotic genes in inflammatory bowel disease; A localized event?Frontiers in immunology · 2022Article
Corrections and comments
- Retraction · 2024-02-20Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Original Data and/or Images not Provided and/or not Available · · See also: https://pubpeer.com/publications/3326AB0A2B1129BA4D39C89BD6EC57
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Psoriasis is a common chronic immune-mediated disease that often has a serious negative impact on the physical and mental health of patients. Dihydroartemisinin (DHA) is a drug with anti-fibrotic and anti-inflammatory effects that may be involved in the autoimmune regulation of immune diseases. However, the effects of DHA on psoriasis have not been reported comprehensively. Therefore, the aim of this study was to investigate the effect of DHA on abnormal proliferation and inflammation of epidermal keratinocyte cells in psoriasis and its mechanism of action. IL-17A-induced human epidermal keratin-forming cells (HaCaT) were used as a model. And after induction exposure to different concentrations of DHA, CCK-8, EDU staining, wound healing and Western blotting were performed to assess cell viability, proliferation, migration, differentiation and inflammatory factors, respectively. Subsequently, agonists of fibroblast growth factor receptor 1 (FGFR1) were added and the above experiments were repeated. The results showed that DHA obviously inhibited IL-17A-induced hyperproliferation, migration and expression of inflammatory factors in HaCaT cells. Furthermore, FGFR1 was highly expressed in IL-17A-induced HaCaT cells, and DHA inhibited its expression. However, the inhibitory effect of DHA on IL-17A-induced HaCaT cells was reversed after the addition of FGFR1 agonist. In conclusion, DHA could inhibit IL-17A-induced hyperproliferation and inflammation of keratinocytes by targeting FGFR1, which also provided a new target for the treatment of psoriasis.
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