Evidence map›Paper›PMID 31712723›Full record

ReviewNature reviews. Rheumatology2019

Shared and distinct mechanisms of fibrosis.

Jörg H W Distler, Andrea-Hermina Györfi, Meera Ramanujam, Michael L Whitfield, Melanie Königshoff, Robert Lafyatis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 389 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
389citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

389 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Review
  10. Broadening horizons: Pathogenesis and therapeutics of renal ciliopathies.Journal of cell communication and signaling · 2026
    Review
  11. Article
  12. Review
  13. Inter-Organ Communication in Pulmonary Fibrosis: Systemic Modifiers of a Lung-Centered Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
    Review
  19. Article
  20. Review

329 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

6 authors.

Jörg H W DistlerDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany. joerg.distler@uk-erlangen.de.ORCID http://orcid.org/0000-0001-7408-9333
Andrea-Hermina GyörfiDepartment of Internal Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg (FAU) and University Hospital Erlangen, Erlangen, Germany.ORCID http://orcid.org/0000-0002-4960-3369
Meera RamanujamImmunology and Respiratory Diseases Research, Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT, USA.
Michael L WhitfieldDepartment of Biomedical Data Science, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA.
Melanie KönigshoffLung Repair and Regeneration Unit, Helmholtz Zentrum München, Ludwig-Maximilians University, University Hospital Großhadern, Member of the German Center for Lung Research (DZL), Munich, Germany.
Robert LafyatisDivision of Rheumatology, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is defined as an excessive deposition of connective tissue components and can affect virtually every organ system, including the skin, lungs, liver and kidney. Fibrotic tissue remodelling often leads to organ malfunction and is commonly associated with high morbidity and mortality. The medical need for effective antifibrotic therapies is thus very high. However, the extraordinarily high costs of drug development and the rare incidence of many fibrotic disorders hinder the development of targeted therapies for individual fibrotic diseases. A potential strategy to overcome this challenge is to target common mechanisms and core pathways that are of central pathophysiological relevance across different fibrotic diseases. The factors influencing susceptibility to and initiation of these diseases are often distinct, with disease-specific and organ-specific risk factors, triggers and sites of first injury. Fibrotic remodelling programmes with shared fibrotic signalling responses such as transforming growth factor-β (TGFβ), platelet-derived growth factor (PDGF), WNT and hedgehog signalling drive disease progression in later stages of fibrotic diseases. The convergence towards shared responses has consequences for drug development as it might enable the development of general antifibrotic compounds that are effective across different disease entities and organs. Technological advances, including new models, single-cell technologies and gene editing, could provide new insights into the pathogenesis of fibrotic diseases and the development of drugs for their treatment.

Indexed as

Connective Tissue DiseasesDisease ManagementGenetic Predisposition to DiseaseImmunity, CellularAnimalsExtracellular Matrix ProteinsFibrosisHumansImmunologic FactorsExtracellular Matrix ProteinsImmunologic Factors

Identifiers

What Socratic 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 Socratic graph.