Evidence map›Paper›PMID 7628865›Full record

ArticleInflammation1995

Modulation of inflammatory arthritis by inhibition of poly(ADP ribose) polymerase.

R Miesel, M Kurpisz, H Kröger

Registry-linked trialAbstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06640309 (The Effect of Nicotinamide on the Clinical Outcome of Rheumatoid Arthritis Patients), which is not on this map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 15% 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.

NCT06640309 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

The Effect of Nicotinamide on the Clinical Outcome of Rheumatoid Arthritis Patients

TypeinterventionalSponsorAin Shams UniversityRan2023 to 2025Enrolled70ConditionsRheumatoid ArthritisArmsNicotinamide Tablet, conventional synthetic antirheumatic drugs
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Diverse therapeutic efficacies and more diverse mechanisms of nicotinamide.Metabolomics : Official journal of the Metabolomic Society · 2019
    Review
  7. Review
  8. Review
  9. PARP-1 hyperactivation and reciprocal elevations in intracellular Ca2+ during ROS-induced nonapoptotic cell death.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Neutrophil apoptosis in autoimmunity.Journal of molecular medicine (Berlin, Germany) · 2006
    Review
  17. Article
  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

3 authors at 2 institutions in 3 countries.

R MieselDepartment of Biochemistry, Deutsches RheumaForschungsZentrum, Berlin, Germany.
M Kurpisz
H Kröger
German Rheumatism Research Centre · DEPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly(ADPR) polymerase (PARP; EC 2.4.2.30) is a nuclear enzyme, which, when activated by oxygen- and nitrogen-radical-induced DNA strand breaks, transfers ADP ribose units to nuclear proteins and initiates apoptosis by depletion of cellular NAD and ATP pools. The present study investigates whether the oxidative stress-dependent activation of PARP plays a role in the etiopathogenesis of arthritis. The antiarthritic reactivity of the biogenic PARP inhibitor nicotinamide was tested in DBA/1 x B10A(4R) mice suffering from potassium peroxochromate-induced arthritis. Daily doses of 4 mmol/kg of NA suppressed the arthritis by 35% and inhibited the phagocytic generation of reactive oxygen species, which increases sixfold during the development of arthritis. The onset, progression, and remission of arthritis correlated positively to the phorbolester-activated respiratory burst of neutrophils and monocytes, and a dose-dependent inhibition of NADPH oxidase activity was determined with human phagocytes. Our data support the hypothesis that oxidative stress-induced alterations in cellular signal transduction pathways play a pivotal role in the development of arthritis, which can be suppressed by the simultaneous inhibition of poly(ADPR) polymerase and NADPH oxidase.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsAnimalsApoptosisArthritisChromatesEnzyme ActivationHumansLuminescent MeasurementsMaleMiceMice, Inbred DBANADH, NADPH OxidoreductasesNADPH OxidasesNiacinamideOxidative StressPeroxidesChromatesNADH, NADPH OxidoreductasesNADPH OxidasesNiacinamidePeroxidesPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerasespotassium tetraperoxochromateReactive Oxygen SpeciesTetradecanoylphorbol Acetate

Identifiers

PMID7628865
OpenAlexW2070754144

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.