Evidence map›Paper›PMID 33983569›Full record

ReviewImmunologic research2021

The p53 status in rheumatoid arthritis with focus on fibroblast-like synoviocytes.

Mahdi Taghadosi, Mehrnoosh Adib, Ahmadreza Jamshidi, Mahdi Mahmoudi, Elham Farhadi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Transcription-based comparison ofMicrobiology spectrum · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Iron metabolism in rheumatic diseases.Journal of translational autoimmunity · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Inhibition of ASIC1a reduces ferroptosis in rheumatoid arthritis articular chondrocytes via the p53/NRF2/SLC7A11 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  16. Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. 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

5 authors at 3 institutions in 1 country.

Mahdi TaghadosiImmunology Department, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Mehrnoosh AdibImmunology Department, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Ahmadreza JamshidiRheumatology Research Center, Shariati Hospital, Tehran University of Medical Sciences, Kargar Ave, PO-BOX: 1411713137, Tehran, Iran.
Mahdi MahmoudiRheumatology Research Center, Shariati Hospital, Tehran University of Medical Sciences, Kargar Ave, PO-BOX: 1411713137, Tehran, Iran. mahmoudim@tums.ac.ir.
Elham FarhadiRheumatology Research Center, Shariati Hospital, Tehran University of Medical Sciences, Kargar Ave, PO-BOX: 1411713137, Tehran, Iran. farhadie@tums.ac.ir.
Kermanshah University of Medical Sciences · IRTehran University of Medical Sciences · IRShariati Hospital · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

P53 is a transcription factor that regulates many signaling pathways like apoptosis, cell cycle, DNA repair, and cellular stress responses. P53 is involved in inflammatory responses through the regulation of inflammatory signaling pathways, induction of cytokines, and matrix metalloproteinase expression. Also, p53 regulates immune responses through modulating Toll-like receptors expression and innate and adaptive immune cell differentiation and maturation. P53 is a modulator of the apoptosis and proliferation processes through regulating multiple anti and pro-apoptotic genes. Rheumatoid arthritis (RA) is categorized as an invasive inflammatory autoimmune disease with irreversible deformity of joints and bone resorption. Different immune and non-immune cells contribute to RA pathogenesis. Fibroblast-like synoviocytes (FLSs) have been recently introduced as a key player in the pathogenesis of RA. These cells in RA synovium produce inflammatory cytokines and matrix metalloproteinases which results in synovitis and joint destruction. Besides, hyper proliferation and apoptosis resistance of FLSs lead to synovial hyperplasia and bone and cartilage destruction. Given the critical role of p53 in inflammation, apoptosis, and cell proliferation, lack of p53 function (due to mutation or low expression) exerts a prominent role for this gene in the pathogenesis of RA. This review focuses on the role of p53 in different mechanisms and cells (specially FLSs) that involved in RA pathogenesis.

Indexed as

AnimalsApoptosisArthritis, ExperimentalArthritis, RheumatoidCartilage, ArticularCell ProliferationCytokinesDNA MethylationEpigenesis, GeneticHumansHyperplasiaLoss of Function MutationMatrix MetalloproteinasesMiceSignal TransductionSynovial MembraneCytokinesMatrix MetalloproteinasesTP53 protein, humanTrp53 protein, mouseTumor Suppressor Protein p53Autoimmune diseasesEpigeneticExpressionMutationP53Rheumatoid arthritis

Identifiers

PMID33983569
OpenAlexW3161154828

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.