Evidence map›Paper›PMID 24577098›Full record

ArticleAutophagy2014

FGF7/KGF regulates autophagy in keratinocytes: A novel dual role in the induction of both assembly and turnover of autophagosomes.

Francesca Belleudi, Valeria Purpura, Silvia Caputo, Maria Rosaria Torrisi

Open access · hybridAbstract read
In one paragraph

Article in Autophagy, 2014. 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
1.3field-weighted citation impact, top 21% 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, 34 citations in OpenAlex.

  1. Review
  2. Trifolirhizin improves the hyperproliferation and excessive inflammatory response in human HaCaT keratinocytes and ameliorates skin lesions in psoriasis-like mouse models.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
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  12. MicroRNAs-103/107 Regulate Autophagy in the Epidermis.The Journal of investigative dermatology · 2018
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  20. The Yin and Yang dualistic features of autophagy in thermal burn wound healing.International journal of immunopathology and pharmacology
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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

4 authors at 1 institution in 1 country.

Francesca BelleudiIstituto Pasteur-Fondazione Cenci Bolognetti; Dipartimento di Medicina Clinica e Molecolare; Sapienza Università di Roma; Rome, Italy.
Valeria PurpuraIstituto Pasteur-Fondazione Cenci Bolognetti; Dipartimento di Medicina Clinica e Molecolare; Sapienza Università di Roma; Rome, Italy.
Silvia CaputoIstituto Pasteur-Fondazione Cenci Bolognetti; Dipartimento di Medicina Clinica e Molecolare; Sapienza Università di Roma; Rome, Italy.
Maria Rosaria TorrisiIstituto Pasteur-Fondazione Cenci Bolognetti; Dipartimento di Medicina Clinica e Molecolare; Sapienza Università di Roma; Rome, Italy; Azienda Ospedaliera S. Andrea; Rome, Italy.
Sapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a degradative pathway through which cells overcome stressful conditions and rapidly change their phenotype during differentiation. Despite its protective role, when exacerbated, autophagy may lead to cell death. Several growth factors involved in cell survival and in preventing differentiation are able to inhibit autophagy. Here we investigated the autophagic role of FGF7/KGF, an important player in epithelial cell protection and differentiation. Biochemical and quantitative fluorescence approaches showed that FGF7 and its signaling induce autophagy in human keratinocytes and the use of specific inhibitors indicated that this effect is independent of the PI3K-AKT-MTOR pathway. The selective block of autophagosome-to-lysosome fusion clarified that FGF7 induces autophagy stimulating autophagosome formation. However, quantitative fluorescence approaches also indicated that, upon a prolonged autophagic stimulus, FGF7 is able to accelerate autophagosome turnover. Moreover, in differentiating keratinocytes, the use of the autophagic inhibitor 3-MA as well as the depletion of BECN1 and ATG5, 2 essential regulators of the process, counteracted the FGF7-induced increase of the differentiation marker KRT1/K1, suggesting that autophagy is required for the FGF7-mediated early differentiation. These results provide the first evidence of a role of FGF7 in the regulation of sequential steps of the autophagic process and strengthen the hypothesis of a direct interplay between autophagy and differentiation. On the other hand, the ability of FGF7 to accelerate autophagosome turnover, preventing their dangerous accumulation, is consistent with the well-established protective role played by the growth factor in epithelial cells.

Indexed as

AutophagyCell DifferentiationCells, CulturedFibroblast Growth Factor 7HumansKeratinocytesLysosomesMembrane FusionPhagosomesFGF7 protein, humanFibroblast Growth Factor 7autophagyFGF7FGFR2bKGFKGFR

Identifiers

PMID24577098
PMCPMC5119059
OpenAlexW1560389661

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.