Evidence map›Paper›PMID 37344157›Full record

ArticleAnnals of the rheumatic diseases2023

Metabolic rewiring controlled by c-Fos governs cartilage integrity in osteoarthritis.

Kazuhiko Matsuoka, Latifa Bakiri, Martin Bilban, Stefan Toegel, Arvand Haschemi, Hao Yuan, Maria Kasper, Reinhard Windhager, Erwin F Wagner

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 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

9 authors at 3 institutions in 2 countries.

Kazuhiko MatsuokaGenes and Disease group, Department of Dermatology, Medical University of Vienna, Vienna, Austria.
Latifa BakiriGenes and Disease group, Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-6300-2420
Martin BilbanDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Stefan ToegelDepartment of Orthopedics and Trauma Surgery, Medical University of Vienna, Vienna, Austria.
Arvand HaschemiDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Hao YuanDepartment of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
Maria KasperDepartment of Cell and Molecular Biology, Karolinska Institute, Stockholm, Sweden.
Reinhard WindhagerDepartment of Orthopedics and Trauma Surgery, Medical University of Vienna, Vienna, Austria.
Erwin F WagnerGenes and Disease group, Department of Dermatology, Medical University of Vienna, Vienna, Austria erwin.wagner@meduniwien.ac.at.ORCID 0000-0001-7872-0196
Medical University of Vienna · ATKarolinska Institutet · SELudwig Boltzmann Institute for Traumatology, The Research Center in Cooperation with AUVA · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThe activator protein-1 (AP-1) transcription factor component c-Fos regulates chondrocyte proliferation and differentiation, but its involvement in osteoarthritis (OA) has not been functionally assessed.

methodsc-Fos expression was evaluated by immunohistochemistry on articular cartilage sections from patients with OA and mice subjected to the destabilisation of the medial meniscus (DMM) model of OA. Cartilage-specific c-Fos knockout (c-Fos

resultsFOS-positive chondrocytes were increased in human and murine OA cartilage during disease progression. Compared with c-Fos

conclusionsc-Fos modulates cellular bioenergetics in chondrocytes by balancing pyruvate flux between anaerobic glycolysis and the tricarboxylic acid cycle in response to OA signals. We identify a novel metabolic adaptation of chondrocytes controlled by c-Fos-containing AP-1 dimers that could be therapeutically relevant.

Indexed as

Cartilage, ArticularOsteoarthritisProto-Oncogene Proteins c-fosAnimalsChondrocytesCollagenDisease Models, AnimalHumansMiceTranscription Factor AP-1CollagenFOS protein, humanFos protein, mouseProto-Oncogene Proteins c-fosTranscription Factor AP-1Arthritis, ExperimentalChondrocytesOsteoarthritis

Identifiers

PMID37344157
PMCPMC10423482
OpenAlexW4381480810

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.