Evidence map›Paper›PMID 16549783›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Galectin-3 regulates myofibroblast activation and hepatic fibrosis.

Neil C Henderson, Alison C Mackinnon, Sarah L Farnworth, Francoise Poirier, Francesco P Russo, John P Iredale, Christopher Haslett, Kenneth J Simpson, Tariq Sethi

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03413072 (Galectin-3 as a Predictor for Thromboembolic Formation in Patients With Non Valvular Atrial Fibrillation Assessed by CHA₂DS₂-VASc Scoring), which is not on this map. Cited by 305 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
305citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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.

NCT03413072 unknown statusnot on this mapstarted 2018, after this paper: background citation

Galectin-3 as a Predictor for Thromboembolic Formation in Patients With Non Valvular Atrial Fibrillation Assessed by CHA₂DS₂-VASc Scoring

TypeobservationalSponsorAssiut UniversityRan2018 to 2020Enrolled140ConditionsAtrial Fibrillation, Stroke
3 · Its place in the literature

Who cites it

305 citing papers in PubMed, 1 synthesis or guideline pooled it, 608 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  5. Trial
  6. Article
  7. Article
  8. Drug Development for MASH-Related Compensated Cirrhosis: Past, Present and Future.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. The Historiography of Galactose and Its Recognition by Galectins.Advances in experimental medicine and biology · 2026
    Review
  19. Article
  20. Review

245 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

9 authors at 3 institutions in 2 countries.

Neil C HendersonCentre for Inflammation Research, Queens Medical Research Institute, University of Edinburgh, 51 Little France Crescent, EH16 4SA Edinburgh, Scotland, United Kingdom.
Alison C Mackinnon
Sarah L Farnworth
Francoise Poirier
Francesco P Russo
John P Iredale
Christopher Haslett
Kenneth J Simpson
Tariq Sethi
Centre for Inflammation Research · GBUniversity of Edinburgh · GBInstitut Jacques Monod · FR

Funding

Medical Research Council G0600033Wellcome Trust
6 · The paper itself

Abstract

Central to fibrogenesis and the scarring of organs is the activation of fibroblasts into matrix-secreting myofibroblasts. We demonstrate that Galectin-3 expression is up-regulated in established human fibrotic liver disease and is temporally and spatially related to the induction and resolution of experimental hepatic fibrosis. Disruption of the Galectin-3 gene blocks myofibroblast activation and procollagen (I) expression in vitro and in vivo, markedly attenuating liver fibrosis. Addition of exogenous recombinant Galectin-3 in vitro reversed this abnormality. The reduction in hepatic fibrosis observed in the Galectin-3(-/-) mouse occurred despite equivalent liver injury and inflammation, and similar tissue expression of TGF-beta. TGF-beta failed to transactivate Galectin-3(-/-) hepatic stellate cells, in contrast with WT hepatic stellate cells; however, TGF-beta-stimulated Smad-2 and -3 activation was equivalent. These data suggest that Galectin-3 is required for TGF-beta mediated myofibroblast activation and matrix production. Finally, in vivo siRNA knockdown of Galectin-3 inhibited myofibroblast activation after hepatic injury and may therefore provide an alternative therapeutic approach to the prevention and treatment of liver fibrosis.

Indexed as

AnimalsCarbon TetrachlorideFibroblastsGalectin 3HumansInflammationLiverLiver CirrhosisLiver Cirrhosis, ExperimentalMiceMice, KnockoutMuscle CellsRatsRNA, Small InterferingSignal TransductionSmad ProteinsCarbon TetrachlorideGalectin 3RNA, Small InterferingSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID16549783
PMCPMC1458794
OpenAlexW2090158969

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.