Evidence map›Paper›PMID 29164267›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2018

Intracellular apoptotic pathways: a potential target for reducing joint damage in rheumatoid arthritis.

Bonnie Williams, Anak Dharmapatni, Tania Crotti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. [Diagnostic value of P2X7 receptor and its role in inflammatory reaction in rheumatoid arthritis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    Article
  8. Review
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 1 institution in 1 country.

Bonnie WilliamsAdelaide Medical School, The University of Adelaide, Adelaide, SA, Australia. bonnie.williams@adelaide.edu.au.ORCID http://orcid.org/0000-0002-2356-105X
Anak DharmapatniAdelaide Medical School, The University of Adelaide, Adelaide, SA, Australia.
Tania CrottiAdelaide Medical School, The University of Adelaide, Adelaide, SA, Australia.
The University of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that results in both local and systemic bone erosion, causing significant joint deformities and functional disability. The increased number of synovial fibroblasts, inflammatory cells and osteoclasts in RA is associated with reduced apoptosis in these cells. The ability to modulate the cell proliferation or death (particularly apoptosis) is recognised for its immense therapeutic potential. Identifying new therapeutics to assist in stimulating apoptosis within the synovial joints therefore may be beneficial in reducing inflammation and bone loss in RA patients. In this review, the roles of anti-apoptotic proteins that are upregulated in RA synovial joints will be discussed in relation to their actions on bone destruction and inflammation. Evidence recently published suggests that intracellular apoptotic inhibitory molecules can be targeted by current or new therapeutics to reduce joint damage in RA. However, the therapeutics that target these molecules are yet to reach clinical trial stages. Even so it is evident that understanding the upregulation of anti-apoptotic molecules in RA is required to improve treatments currently available for RA patients.

Indexed as

ApoptosisAnimalsArthritis, RheumatoidHumansSignal TransductionAnti-apoptotic proteinsApoptosisBone erosionDisease-modifying anti-rheumatic drugsRheumatoid arthritisTherapeutics

Identifiers

PMID29164267
OpenAlexW2768830462

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.