Evidence map›Paper›PMID 27247426›Full record

ReviewBioscience reports2016

Involvement of matrix metalloproteinases (MMPs) and inflammasome pathway in molecular mechanisms of fibrosis.

Sacha Robert, Thomas Gicquel, Tatiana Victoni, Samuel Valença, Emiliano Barreto, Béatrice Bailly-Maître, Elisabeth Boichot, Vincent Lagente

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
11.3field-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

82 citing papers in PubMed, 180 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Targeting macrophages in liver fibrosis.Frontiers in immunology · 2026
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22 more citing papers are in PubMed but not listed here.

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

8 authors at 5 institutions in 2 countries.

Sacha RobertUMR991 INSERM, Université de Rennes 1, 35043 Rennes, France.
Thomas GicquelUMR991 INSERM, Université de Rennes 1, 35043 Rennes, France.
Tatiana VictoniLaboratório de Reparo Tecidual, DHE/IBRAG/UERJ, 20550-170 Rio de Janeiro, Brazil.
Samuel ValençaInstituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, 21941-902 Rio de Janeiro, Brazil.
Emiliano BarretoLaboratory of Cell Biology, Federal University of Alagoas, 57072-900 Maceió-AL, Brazil.
Béatrice Bailly-MaîtreINSERM, U1065, Faculté de Médecine, Université de Nice Sophia Antipolis, 06204 Nice, France.
Elisabeth BoichotUMR991 INSERM, Université de Rennes 1, 35043 Rennes, France.
Vincent LagenteUMR991 INSERM, Université de Rennes 1, 35043 Rennes, France vincent.lagente@univ-rennes1.fr.
Inserm · FRUniversidade Federal de Alagoas · BRUniversidade Federal do Rio de Janeiro · BRUniversité Côte d'Azur · FRUniversité de Rennes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is a basic connective tissue lesion defined by the increase in the fibrillar extracellular matrix (ECM) components in tissue or organ. Matrix metalloproteinases (MMPs) are a major group of proteases known to regulate the turn-over of ECM and so they are suggested to be important in tissue remodelling observed during fibrogenic process associated with chronic inflammation. Tissue remodelling is the result of an imbalance in the equilibrium of the normal processes of synthesis and degradation of ECM components markedly controlled by the MMPs/TIMP imbalance. We previously showed an association of the differences in collagen deposition in the lungs of bleomycin-treated mice with a reduced molar pro-MMP-9/TIMP-1 ratio. Using the carbon tetrachloride (CCl4) preclinical model of liver fibrosis in mice, we observed a significant increase in collagen deposition with increased expression and release of tissue inhibitors of metalloproteinase (TIMP)-1 both at 24 h and 3 weeks later. This suggests an early altered regulation of matrix turnover involved in the development of fibrosis. We also demonstrated an activation of NLRP3-inflammasome pathway associated with the IL-1R/MyD88 signalling in the development of experimental fibrosis both in lung and liver. This was also associated with an increased expression of purinergic receptors mainly P2X7 Finally, these observations emphasize those effective therapies for these disorders must be given early in the natural history of the disease, prior to the development of tissue remodelling and fibrosis.

Indexed as

AnimalsFibrosisHumansInflammasomesInflammationMatrix MetalloproteinasesSignal TransductionTissue Inhibitor of Metalloproteinase-1InflammasomesMatrix MetalloproteinasesTissue Inhibitor of Metalloproteinase-1fibrosisinflammasomeinterleukin-1liverlungmatrix metalloproteinasepurinergic receptorstissue inhibitors of metalloproteinase (TIMP)-1

Identifiers

PMID27247426
PMCPMC4945993
OpenAlexW2414895309

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.