Evidence map›Paper›PMID 37039837›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis.

Tazio Maleitzke, Tamara Dietrich, Alexander Hildebrandt, Jérôme Weber, Jessika Appelt, Denise Jahn, Ellen Otto, Dario Zocholl, Shan Jiang, Anke Baranowsky and 3 more

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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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

13 authors at 3 institutions in 1 country.

Tazio MaleitzkeCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0003-2924-7384
Tamara DietrichCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.
Alexander HildebrandtCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0003-3560-1642
Jérôme WeberCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0003-3829-9397
Jessika AppeltCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0001-6351-9959
Denise JahnCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0001-8912-5851
Ellen OttoCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0001-9394-0066
Dario ZochollCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Institute of Biometry and Clinical Epidemiology, Berlin, Germany.ORCID http://orcid.org/0000-0002-9218-6919
Shan JiangUniversity Medical Center Hamburg-Eppendorf, Department of Trauma and Orthopedic Surgery, Hamburg, Germany.ORCID http://orcid.org/0000-0002-1545-2152
Anke BaranowskyUniversity Medical Center Hamburg-Eppendorf, Department of Trauma and Orthopedic Surgery, Hamburg, Germany.
Georg N DudaBerlin Institute of Health at Charité - Universitätsmedizin Berlin, Julius Wolff Institute, Berlin, Germany.ORCID http://orcid.org/0000-0001-7605-3908
Serafeim TsitsilonisCharité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Center for Musculoskeletal Surgery, Berlin, Germany.ORCID http://orcid.org/0000-0002-6529-6864
Johannes KellerUniversity Medical Center Hamburg-Eppendorf, Department of Trauma and Orthopedic Surgery, Hamburg, Germany. j.keller@uke.de.ORCID http://orcid.org/0000-0002-8925-7288
Humboldt-Universität zu Berlin · DEUniversität Hamburg · DEBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DE

Funding

Deutsche Forschungsgemeinschaft KE 2179/2-1Deutsche Forschungsgemeinschaft TS 303/2-1Else Kröner-Fresenius-Stiftung EKFS 2017_A22Stiftung Oskar-Helene-Heim OHH_44
6 · The paper itself

Abstract

backgroundProcalcitonin (PCT) is applied as a sensitive biomarker to exclude bacterial infections in patients with rheumatoid arthritis (RA) flare-ups. Beyond its diagnostic value, little is known about the pathophysiological role of PCT in RA.

methodsCollagen antibody-induced arthritis (CAIA) was induced in Calca-deficient mice (Calca

resultsSerum PCT levels and intra-articular PCT expression increased following CAIA induction. While WT animals developed a full arthritic phenotype, Calca-deficient mice were protected from clinical and histological signs of arthritis and grip strength was preserved. Cartilage turnover markers and Tnfa were exclusively elevated in WT mice. Calca-deficient animals expressed increased levels of Il1b. Decreased bone surface and increased subchondral bone porosity were observed in WT mice, while Calca-deficiency preserved bone integrity.

conclusionThe inactivation of Calca and thereby PCT provided full protection from joint inflammation and arthritic bone loss in mice exposed to CAIA. Together with our previous findings on the pathophysiological function of Calca-derived peptides, these data indicate an independent pro-inflammatory role of PCT in RA.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidAnimalsGenotypeInflammationMiceProcalcitoninProcalcitoninBoneCalcaCartilageJoint inflammationPCTRheumatoid arthritis

Identifiers

PMID37039837
OpenAlexW4364353533

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.