Evidence map›Paper›PMID 26914707›Full record

ReviewThe Journal of membrane biology2016

Connexins, Pannexins, and Their Channels in Fibroproliferative Diseases.

Bruno Cogliati, Gregory Mennecier, Joost Willebrords, Tereza Cristina Da Silva, Michaël Maes, Isabel Veloso Alves Pereira, Sara Crespo-Yanguas, Francisco Javier Hernandez-Blazquez, Maria Lúcia Zaidan Dagli, Mathieu Vinken

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of membrane biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Connexin Expression Is Altered in Liver Development ofInternational journal of molecular sciences · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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

10 authors at 2 institutions in 2 countries.

Bruno Cogliati *Department of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Gregory Mennecier *Department of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Joost WillebrordsDepartment of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Brussels, Belgium.
Tereza Cristina Da SilvaDepartment of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Michaël MaesDepartment of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Brussels, Belgium.
Isabel Veloso Alves PereiraDepartment of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Sara Crespo-YanguasDepartment of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Brussels, Belgium.
Francisco Javier Hernandez-BlazquezDepartment of Surgery, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Maria Lúcia Zaidan DagliDepartment of Pathology, School of Veterinary Medicine and Animal Science, University of São Paulo, Brazil.
Mathieu VinkenDepartment of In Vitro Toxicology and Dermato-Cosmetology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Brussels, Belgium.
Universidade de São Paulo · BRVrije Universiteit Brussel · BE

Funding

European Research Council 335476
6 · The paper itself

Abstract

Cellular and molecular mechanisms of wound healing, tissue repair, and fibrogenesis are established in different organs and are essential for the maintenance of function and tissue integrity after cell injury. These mechanisms are also involved in a plethora of fibroproliferative diseases or organ-specific fibrotic disorders, all of which are associated with the excessive deposition of extracellular matrix components. Fibroblasts, which are key cells in tissue repair and fibrogenesis, rely on communicative cellular networks to ensure efficient control of these processes and to prevent abnormal accumulation of extracellular matrix into the tissue. Despite the significant impact on human health, and thus the epidemiologic relevance, there is still no effective treatment for most fibrosis-related diseases. This paper provides an overview of current concepts and mechanisms involved in the participation of cellular communication via connexin-based pores as well as pannexin-based channels in the processes of tissue repair and fibrogenesis in chronic diseases. Understanding these mechanisms may contribute to the development of new therapeutic strategies to clinically manage fibroproliferative diseases and organ-specific fibrotic disorders.

Indexed as

AnimalsCell CommunicationConnexinsDisease SusceptibilityFibroblastsFibrosisGap JunctionsGene Expression RegulationHumansLiverMyocardiumOrgan SpecificitySignal TransductionSkinWound HealingConnexinsCellular communicationFibrosisFibrotic diseasesTissue repairWound healing

Identifiers

PMID26914707
PMCPMC5417354
OpenAlexW2279126440

What OpenQuestion holds

Textmetadata
LicenceTDM
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.