Evidence map›Paper›PMID 35809213›Full record

ReviewCurrent rheumatology reports2022

Deep Insight into the Role of MIF in Spondyloarthritis.

Brian Wu, Akihiro Nakamura

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

2 authors at 1 institution in 1 country.

Brian WuSchroeder Arthritis Institute, University Health Network, 60 Leonard Avenue, Toronto, ON, M5T 0S8, Canada.
Akihiro NakamuraSchroeder Arthritis Institute, University Health Network, 60 Leonard Avenue, Toronto, ON, M5T 0S8, Canada. Akihiro.Nakamura@uhnresearch.ca.ORCID 0000-0002-4258-1603
University Health Network · CA

Funding

CIHR
6 · The paper itself

Abstract

purpose of reviewPathological roles of macrophage migration inhibitory factor (MIF) have recently been demonstrated in spondyloarthritis (SpA) preclinical models, identifying MIF as a new treatment target for SpA. However, the specific contribution of MIF and therapeutic potential of MIF-targeted therapies to various tissue types affected by SpA are not well delineated. RECENT

findingsMIF and its cognate receptor CD74 are extensively involved in the pathogenesis of SpA including inflammation in the spine, joint, eyes, skin, and gut. The majority of the current evidence has consistently shown that MIF drives the inflammation in these distinct anatomical sites. In preclinical models, genetic deletion or blockade of MIF reduces the severity of inflammation. Although MIF is generally an upstream cytokine which regulates downstream effector cytokines, MIF also intensifies type 3 immunity by promoting helper T 17 (Th17) plasticity. MIF- or CD74-targeted therapies have also reported to be well tolerated in clinical trials for other diseases. Recent findings suggest that MIF-CD74 axis is a new therapeutic target for SpA to improve various clinical features. Clinical trials for MIF- or CD74-targeted therapies for SpA patients are warranted.

Indexed as

Macrophage Migration-Inhibitory FactorsSpondylarthritisHumansInflammationIntramolecular OxidoreductasesIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, humanCD74EnthesitisMacrophage migration inhibitory factorNew bone formationSpondyloarthritisType 3 immunity

Identifiers

PMID35809213
OpenAlexW4284970413

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.