Evidence map›Paper›PMID 35078974›Full record

ArticleBone research2022

Theobroma cacao improves bone growth by modulating defective ciliogenesis in a mouse model of achondroplasia.

Ludovic Martin, Nabil Kaci, Catherine Benoist-Lasselin, Marine Mondoloni, Suzanne Decaudaveine, Valentin Estibals, Maxence Cornille, Léa Loisay, Justine Flipo, Benoît Demuynck and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 11 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

17 authors at 4 institutions in 3 countries.

Ludovic Martin *Université de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.ORCID http://orcid.org/0000-0002-4325-6765
Nabil Kaci *Université de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Catherine Benoist-Lasselin *Université de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Marine MondoloniUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Suzanne DecaudaveineUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Valentin EstibalsUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Maxence CornilleUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Léa LoisayUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Justine FlipoUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Benoît DemuynckUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Maria de la Luz Cádiz-GurreaDepartment of Analytical Chemistry, University of Granada, Granada, Spain.
Florent BarbaultUniversité de Paris, ITODYS, CNRS, UMR 7086, 15 rue J-A de Baïf, Paris, France.
Salvador Fernández-ArroyoDepartment of Analytical Chemistry, University of Granada, Granada, Spain.
Laurent SchiblerALLICE, Maison Nationale des Eleveurs, Paris, France.
Antonio Segura-CarreteroDepartment of Analytical Chemistry, University of Granada, Granada, Spain.
Emilie DambroiseUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France.
Laurence Legeai-MalletUniversité de Paris, Imagine Institute, Laboratory of Molecular and Physiopathological Bases of Osteochondrodysplasia, INSERM UMR 1163, F‑75015, Paris, France. laurence.legeai-mallet@inserm.fr.
Inserm · FRUniversidad de Granada · ESCentre National de la Recherche Scientifique · FRMaison des Sciences de l'Homme · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A gain-of-function mutation in the fibroblast growth factor receptor 3 gene (FGFR3) results in achondroplasia (ACH), the most frequent form of dwarfism. Constitutive activation of FGFR3 impairs bone formation and elongation and many signal transduction pathways. Identification of new and relevant compounds targeting the FGFR3 signaling pathway is of broad importance for the treatment of ACH, and natural plant compounds are prime drug candidate sources. Here, we found that the phenolic compound (-)-epicatechin, isolated from Theobroma cacao, effectively inhibited FGFR3's downstream signaling pathways. Transcriptomic analysis in an Fgfr3 mouse model showed that ciliary mRNA expression was modified and influenced significantly by the Indian hedgehog and PKA pathways. (-)-Epicatechin is able to rescue mRNA expression impairments that control both the structural organization of the primary cilium and ciliogenesis-related genes. In femurs isolated from a mouse model (Fgfr3

Identifiers

PMID35078974
PMCPMC8789790
OpenAlexW4226423044

What OpenQuestion holds

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Registered trials

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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.