Evidence map›Paper›PMID 33425206›Full record

ArticleOxidative medicine and cellular longevity2020

Azelaic Acid Exerts Antileukemia Effects against Acute Myeloid Leukemia by Regulating the Prdxs/ROS Signaling Pathway.

Dongdong Zhang, Ziyi Luo, Yanxia Jin, Yanling Chen, Tian Yang, Qian Yang, Balu Wu, Yufeng Shang, Xiaoyan Liu, Yongchang Wei and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  9. Review
  10. Role of reactive oxygen species in myelodysplastic syndromes.Cellular & molecular biology letters · 2024
    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

11 authors at 2 institutions in 1 country.

Dongdong Zhang *Department of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0001-7611-3114
Ziyi Luo *Department of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0003-1884-1484
Yanxia JinDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.
Yanling ChenDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.
Tian YangDepartment of Radiation and Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan 430071, China.
Qian YangDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0002-4777-2548
Balu WuDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0002-3758-1465
Yufeng ShangDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.
Xiaoyan LiuDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0003-4557-9362
Yongchang WeiDepartment of Radiation and Medical Oncology, Zhongnan Hospital, Wuhan University, Wuhan 430071, China.ORCID https://orcid.org/0000-0001-7205-4663
Fuling ZhouDepartment of Hematology, Zhongnan Hospital, Wuhan University, No. 169 Donghu Road, Wuchang District, Wuhan, 4300071 Hubei Province, China.ORCID https://orcid.org/0000-0003-0982-0382
Wuhan University · CNHubei University of Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a hematological malignancy with a poor prognosis attributed to elevated reactive oxygen species (ROS) levels. Thus, agents that inhibit ROS generation in AML should be exploited. Azelaic acid (AZA), a small molecular compound, can scavenge ROS and other free radicals, exerting antitumor effects on various tumor cells. Herein, this study evaluated the antileukemic activity of AZA against AML via regulation of the ROS signaling pathway. We found that AZA reduced intracellular ROS levels and increased total antioxidant capacity in AML cell lines and AML patient cells. AZA suppressed the proliferation of AML cell lines and AML patient cells, expending minimal cytotoxicity on healthy cells. Laser confocal microscopy showed that AZA-treated AML cells surged and ruptured gradually on microfluidic chips. Additionally, AZA promoted AML cell apoptosis and arrested the cell cycle at the G1 phase. Further analysis demonstrated that peroxiredoxin (Prdx) 2 and Prdx3 were upregulated in AZA-treated AML cells.

Indexed as

Reactive Oxygen SpeciesAnimalsAntineoplastic AgentsAntioxidantsApoptosisBone MarrowCell Line, TumorCell ProliferationDicarboxylic AcidsFemaleGene Expression Regulation, LeukemicHL-60 CellsHumansImmunophenotypingLeukemia, Myeloid, AcuteMiceAntineoplastic AgentsAntioxidantsazelaic acidDicarboxylic AcidsPeroxiredoxin IIIPeroxiredoxinsPRDX2 protein, humanPRDX3 protein, humanReactive Oxygen Species

Identifiers

PMID33425206
PMCPMC7775164
OpenAlexW3113567857

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.