Evidence map›Paper›PMID 34755840›Full record

ArticleCardiovascular research2022

FGF10 promotes cardiac repair through a dual cellular mechanism increasing cardiomyocyte renewal and inhibiting fibrosis.

Fabien Hubert, Sandy M Payan, Edeline Pelce, Laetitia Bouchard, Rachel Sturny, Nicolas Lenfant, Giovanna Mottola, Frédéric Collart, Robert G Kelly, Francesca Rochais

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. FGF family in health and disease.Molecular biomedicine · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Fabien HubertAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.ORCID 0000-0003-1360-4092
Sandy M PayanAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.
Edeline PelceAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.
Laetitia BouchardAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.
Rachel SturnyAix Marseille Univ, CNRS UMR 7288, IBDM, Campus de Luminy Case 907, CEDEX 9, 13288 Marseille, France.
Nicolas LenfantAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.ORCID 0000-0002-0519-1120
Giovanna MottolaAix-Marseille Univ, C2VN, INSERM 1263, INRAE 1260, 27 Boulevard Jean Moulin, 13005 Marseille, France.ORCID 0000-0002-7541-0472
Frédéric CollartDepartment of Cardiac Surgery, Timone Hospital, AP-HM, 264 rue Saint-Pierre, 13005 Marseille, France.
Robert G KellyAix Marseille Univ, CNRS UMR 7288, IBDM, Campus de Luminy Case 907, CEDEX 9, 13288 Marseille, France.
Francesca RochaisAix-Marseille Univ, INSERM, MMG, U 1251, 27 Boulevard Jean Moulin, 13005 Marseille, France.ORCID 0000-0001-9355-8916
Inserm · FRCentre National de la Recherche Scientifique · FRHôpital de la Timone · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsPromoting cardiomyocyte renewal represents a major therapeutic approach for heart regeneration and repair. Our study aims to investigate the relevance of FGF10 as a potential target for heart regeneration. METHODS AND

resultsOur results first reveal that Fgf10 levels are up-regulated in the injured ventricle after MI. Adult mice with reduced Fgf10 expression subjected to MI display impaired cardiomyocyte proliferation and enhanced cardiac fibrosis, leading to a worsened cardiac function and remodelling post-MI. In contrast, conditional Fgf10 overexpression post-MI revealed that, by enhancing cardiomyocyte proliferation and preventing scar-promoting myofibroblast activation, FGF10 preserves cardiac remodelling and function. Moreover, FGF10 activates major regenerative pathways including the regulation of Meis1 expression levels, the Hippo signalling pathway and a pro-glycolytic metabolic switch. Finally, we demonstrate that elevated FGF10 levels in failing human hearts correlate with reduced fibrosis and enhanced cardiomyocyte proliferation.

conclusionsAltogether, our study shows that FGF10 promotes cardiac regeneration and repair through two cellular mechanisms: elevating cardiomyocyte renewal and limiting fibrosis. This study thus identifies FGF10 as a clinically relevant target for heart regeneration and repair in man.

Indexed as

Myocardial InfarctionMyocytes, CardiacAnimalsCell ProliferationCells, CulturedFibroblast Growth Factor 10FibrosisHumansMiceRegenerationFGF10 protein, humanFgf10 protein, mouseFibroblast Growth Factor 10Cardiomyocyte proliferationFibroblast growth factor FGF10FibrosisHeart regenerationMyocardial infarction

Identifiers

PMID34755840
OpenAlexW3212007850

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.