Evidence map›Paper›PMID 25165568›Full record

ReviewF1000prime reports2014

Pathogenesis of idiopathic pulmonary fibrosis: review of recent findings.

Elisabetta Renzoni, Veeraraghavan Srihari, Piersante Sestini

Open access · bronzeAbstract readReview
In one paragraph

Review in F1000prime reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

  1. Evidence that metformin promotes fibrosis resolutionActa pharmaceutica Sinica. B · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Stem cell-based Lung-on-Chips: The best of both worlds?Advanced drug delivery reviews · 2019
    Review
  9. HeterozygousRespiratory medicine case reports · 2019
    Article
  10. Article
  11. Type 2 macrophages and Th2 CD4+ cells in interstitial lung diseases (ILDs): an overview.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2018
    Review
  12. Article
  13. Lung Pericytes and Resident Fibroblasts: Busy Multitaskers.The American journal of pathology · 2016
    Review
  14. Article
  15. Article
  16. Macrophage polarization in interstitial lung diseases.Central-European journal of immunology · 2016
    Article
  17. Article
  18. Article
  19. FK506-Binding Protein 10, a Potential Novel Drug Target for Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2015
    Article
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

3 authors at 1 institution in 1 country.

Elisabetta RenzoniInterstitial Lung Disease Unit, Royal Brompton Hospital and National Heart and Lung Institute Imperial College London, Emmanuel Kaye Building, 1B Manresa Road, London SW3 6LR UK.
Veeraraghavan SrihariDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care, Emory University 1365 Clifton Rd NE Rm A 4319, Atlanta, GA 30322 USA.
Piersante SestiniRespiratory Medicine Department, Ospedale "Le Scotte", University of Siena, viale Bracci 53100 Siena Italy.
Imperial College London · GB

Funding

Department of Health PB-PG-0712-28073
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is likely to result from the interaction between environmental exposures, including cigarette smoke, and genetic predisposition. This review focuses on clues provided by recent genetic association studies and other selected data and hypotheses. In IPF, association with surfactant mutations has highlighted the importance of type II epithelial cells, while shortened telomeres in some patients suggest that accelerated aging may play a role in the pathogenesis of lung fibrosis, possibly by affecting the renewal/differentiation potential of epithelial cells. The finding that a common variant in mucin 5B predisposes individuals to both familial and sporadic IPF suggests a hitherto under-investigated role of bronchiolar cells and mucins. Although the pathogenetic link between mucins and lung fibrosis is not known, it is possible that MUC5B overexpression interferes with physiological mucosal host defense, with reduced clearance of micro-organisms or inorganic noxious agents, or induction of endoplasmic reticulum stress. Other components of innate and adaptive immunity are likely to be involved in IPF pathogenesis/progression. Finally, the importance of the clotting cascade in IPF pathogenesis has been confirmed by a recent epidemiological study, in which patients with IPF were almost five times more likely than general population controls to have at least one inherited or acquired clotting defect.

Identifiers

PMID25165568
PMCPMC4126534
OpenAlexW1968094283

What OpenQuestion holds

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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.