Evidence map›Paper›PMID 28646516›Full record

ArticleBritish journal of pharmacology2017

Tofacitinib restores the inhibition of reverse cholesterol transport induced by inflammation: understanding the lipid paradox associated with rheumatoid arthritis.

S Pérez-Baos, J I Barrasa, P Gratal, A Larrañaga-Vera, I Prieto-Potin, G Herrero-Beaumont, R Largo

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.0field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

S Pérez-BaosBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
J I BarrasaBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
P GratalBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
A Larrañaga-VeraBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
I Prieto-PotinBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
G Herrero-BeaumontBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.ORCID http://orcid.org/0000-0002-3241-991X
R LargoBone and Joint Research Unit, Rheumatology Department, IIS-Fundación Jiménez Díaz UAM, Madrid, Spain.
Hospital Universitario Fundación Jiménez Díaz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePatients with active rheumatoid arthritis (RA) have increased cardiovascular mortality, paradoxically associated with reduced circulating lipid levels. The JAK inhibitor tofacitinib ameliorates systemic and joint inflammation in RA with a concomitant increase in serum lipids. We analysed the effect of tofacitinib on the lipid profile of hyperlipidaemic rabbits with chronic arthritis (CA) and on the changes in reverse cholesterol transport (RCT) during chronic inflammation. EXPERIMENTAL APPROACH: CA was induced in previously immunized rabbits, fed a high-fat diet, by administering four intra-articular injections of ovalbumin. A group of rabbits received tofacitinib (10 mg·kg KEY

resultsTofacitinib decreased systemic and synovial inflammation and increased circulating lipid levels. Although it did not modify synovial macrophage density, it reduced the lipid content within synovial macrophages. In foam macrophages in culture, IFNγ further stimulated intracellular lipid accumulation, while the JAK/STAT inhibition provoked by tofacitinib induced lipid release by increasing the levels of cellular liver X receptor α and ATP-binding cassette transporter (ABCA1) synthesis. CONCLUSIONS AND IMPLICATIONS: Active inflammation could be associated with lipid accumulation within macrophages of CA rabbits. JAK inhibition induced lipid release through RCT activation, providing a plausible explanation for the effect of tofacitinib on the lipid profile of RA patients.

Indexed as

AnimalsArthritis, RheumatoidCholesterolDiet, High-FatDose-Response Relationship, DrugInflammationLipidsMacrophagesMalePiperidinesPyrimidinesPyrrolesRabbitsStructure-Activity RelationshipCholesterolLipidsPiperidinesPyrimidinesPyrrolestofacitinib

Identifiers

PMID28646516
PMCPMC5573422
OpenAlexW2754250500

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.