Evidence map›Paper›PMID 33260629›Full record

ReviewInternational journal of molecular sciences2020

Effects of Biological Therapies on Molecular Features of Rheumatoid Arthritis.

Chary Lopez-Pedrera, Nuria Barbarroja, Alejandra M Patiño-Trives, Maria Luque-Tévar, Eduardo Collantes-Estevez, Alejandro Escudero-Contreras, Carlos Pérez-Sánchez

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 38 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.

Chary Lopez-PedreraRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.ORCID 0000-0003-2067-4603
Nuria BarbarrojaRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.
Alejandra M Patiño-TrivesRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.
Maria Luque-TévarRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.
Eduardo Collantes-EstevezRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.ORCID 0000-0002-7647-6289
Alejandro Escudero-ContrerasRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.
Carlos Pérez-SánchezRheumatology Service, Reina Sofia Hospital, Maimonides Institute for Research in Biomedicine of Cordoba (IMIBIC), University of Cordoba, E-14004 Córdoba, Spain.
Instituto Maimónides de Investigación Biomédica de Córdoba · ES

Funding

Consejeria de Salud, Junta de Andalucia PI-0285-2017Instituto de Salud Carlos III PI18/0837Instituto de Salud Carlos III RD16/0012/0015
6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune and chronic inflammatory disease primarily affecting the joints, and closely related to specific autoantibodies that mostly target modified self-epitopes. Relevant findings in the field of RA pathogenesis have been described. In particular, new insights come from studies on synovial fibroblasts and cells belonging to the innate and adaptive immune system, which documented the aberrant production of inflammatory mediators, oxidative stress and NETosis, along with relevant alterations of the genome and on the regulatory epigenetic mechanisms. In recent years, the advances in the understanding of RA pathogenesis by identifying key cells and cytokines allowed the development of new targeted disease-modifying antirheumatic drugs (DMARDs). These drugs considerably improved treatment outcomes for the majority of patients. Moreover, numerous studies demonstrated that the pharmacological therapy with biologic DMARDs (bDMARDs) promotes, in parallel to their clinical efficacy, significant improvement in all these altered molecular mechanisms. Thus, continuous updating of the knowledge of molecular processes associated with the pathogenesis of RA, and on the specific effects of bDMARDs in the correction of their dysregulation, are essential in the early and correct approach to the treatment of this complex autoimmune disorder. The present review details basic mechanisms related to the physiopathology of RA, along with the core mechanisms of response to bDMARDs.

Indexed as

Biological TherapyAnimalsArthritis, RheumatoidAutoimmunityHumansInflammationMicroRNAsOxidative StressMicroRNAsautoimmunitybDMARDsepigenetic and pos-transcriptional mechanismsgenomeinflammationNETosisoxidative stressrheumatoid arthritis

Identifiers

PMID33260629
PMCPMC7731249
OpenAlexW3107843858

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.