Evidence map›Paper›PMID 38407703›Full record

ArticleInflammopharmacology2024

Sulfasalazine promotes ferroptosis through AKT-ERK1/2 and P53-SLC7A11 in rheumatoid arthritis.

Chenyu Zhao, Yunyuan Yu, Guangrong Yin, Chao Xu, Jiahao Wang, Liangliang Wang, Gongyin Zhao, Su Ni, Haoxing Zhang, Baojun Zhou and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Inflammopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

31 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Ferroptosis in cancer: molecular mechanisms, biological roles, and therapeutic significance.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  7. Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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  10. Frontiers in microbiology · 2026
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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 7 institutions in 2 countries.

Chenyu Zhao *Department of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Yunyuan Yu *Department of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Guangrong YinDepartment of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Chao XuTruma Central, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Jiahao WangDepartment of Orthopedics, Affiliated Sport Hospital of CDSU (Chengdu Sport University), 251 Wuhouci Street, Chengdu, 610041, China.
Liangliang WangDepartment of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Gongyin ZhaoDepartment of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Su NiMedical Research Center, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China.
Haoxing ZhangGuangdong Provincial Key Laboratory of Genome Stability and Disease Prevention, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, 518055, People's Republic of China.
Baojun ZhouDepartment of Orthopedics, The Third Affiliated Hospital of Gansu University of Chinese Medicine, 222 Silong Road, Baiyin, 730900, China.
Yuji WangDepartment of Orthopedics, The Affiliated Changzhou Second People's Hospital of Nanjing Medical University, Changzhou Medical Center, Nanjing Medical University, 29 Xinglong Alley, Changzhou, 213003, China. 13775221377@139.com.ORCID http://orcid.org/0000-0003-1385-7217
Changzhou No.2 People's Hospital · CNChengdu Sport University · CNDalian Medical University · CNGansu University of Traditional Chinese Medicine · CNMayo Clinic · USMayo Clinic in Arizona · USShenzhen University · CN

Funding

Major Research Project of Changzhou Commission of Health ZD202217National Natural Science Foundation of China 82002321the Clinical Research Project of Changzhou Medical Center of Nanjing Medical University CMCB202208
6 · The paper itself

Abstract

objectiveFerroptosis has been reported to play a role in rheumatoid arthritis (RA). Sulfasalazine, a common clinical treatment for ankylosing spondylitis, also exerts pathological influence on the progression of rheumatoid arthritis including the induced ferroptosis of fibroblast-like synoviocytes (FLSs), which result in the perturbated downstream signaling and the development of RA. The aim of this study was to investigate the underlying mechanism so as to provide novel insight for the treatment of RA.

methodsCCK-8 and Western blotting were used to assess the effect of sulfasalazine on FLSs. A collagen-induced arthritis mouse model was constructed by the injection of collagen and Freund's adjuvant, and then, mice were treated with sulfasalazine from day 21 after modeling. The synovium was extracted and ferroptosis was assessed by Western blotting and immunofluorescence staining.

resultsThe results revealed that sulfasalazine promotes ferroptosis. Compared with the control group, the expression levels of ferroptosis-related proteins such as glutathione peroxidase 4, ferritin heavy chain 1, and solute carrier family 7, member 11 (SLC7A11) were lower in the experimental group. Furthermore, deferoxamine inhibited ferroptosis induced by sulfasalazine. Sulfasalazine-promoted ferroptosis was related to a decrease in ERK1/2 and the increase of P53.

conclusionsSulfasalazine promoted ferroptosis of FLSs in rheumatoid arthritis, and the PI3K-AKT-ERK1/2 pathway and P53-SLC7A11 pathway play an important role in this process.

Indexed as

Arthritis, RheumatoidFerroptosisAnimalsCell ProliferationCells, CulturedMAP Kinase Signaling SystemMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSulfasalazineTumor Suppressor Protein p53Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSulfasalazineTumor Suppressor Protein p53FerroptosisFibroblast-like synoviocyteRheumatoid arthritisSulfasalazine

Identifiers

PMID38407703
PMCPMC11006818
OpenAlexW4392161643

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.