Evidence map›Paper›PMID 24478701›Full record

ReviewFrontiers in pharmacology2013

Are mast cells instrumental for fibrotic diseases?

Catherine Overed-Sayer, Laura Rapley, Tomas Mustelin, Deborah L Clarke

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
    Review
  7. Article
  8. Article
  9. Notch signaling regulates pulmonary fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  10. Review
  11. The molecular mechanisms of remodeling in asthma, COPD and IPF with a special emphasis on the complex role of Wnt5A.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Pathophysiology of systemic sclerosis (scleroderma).The Kaohsiung journal of medical sciences · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. Immune Cells in Subretinal Wound Healing and Fibrosis.Frontiers in cellular neuroscience · 2022
    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

4 authors at 1 institution in 1 country.

Catherine Overed-SayerDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd Cambridge, UK.
Laura RapleyDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd Cambridge, UK.
Tomas MustelinDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd Cambridge, UK.
Deborah L ClarkeDepartment of Respiratory, Inflammation and Autoimmunity, MedImmune Ltd Cambridge, UK.
Institute of Neuroimmunology of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a fatal lung disorder of unknown etiology characterized by accumulation of lung fibroblasts and extracellular matrix deposition, ultimately leading to compromised tissue architecture and lung function capacity. IPF has a heterogeneous clinical course; however the median survival after diagnosis is only 3-5 years. The pharmaceutical and biotechnology industry has made many attempts to find effective treatments for IPF, but the disease has so far defied all attempts at therapeutic intervention. Clinical trial failures may arise for many reasons, including disease heterogeneity, lack of readily measurable clinical end points other than overall survival, and, perhaps most of all, a lack of understanding of the underlying molecular mechanisms of the progression of IPF. The precise link between inflammation and fibrosis remains unclear, but it appears that immune cells can promote fibrosis by releasing fibrogenic factors. So far, however, therapeutic approaches targeting macrophages, neutrophils, or lymphocytes have failed to alter disease pathogenesis. A new cell to garner research interest in fibrosis is the mast cell. Increased numbers of mast cells have long been known to be present in pulmonary fibrosis and clinically correlations between mast cells and fibrosis have been reported. More recent data suggests that mast cells may contribute to the fibrotic process by stimulating fibroblasts resident in the lung, thus driving the pathogenesis of the disease. In this review, we will discuss the mast cell and its physiological role in tissue repair and remodeling, as well as its pathological role in fibrotic diseases such as IPF, where the process of tissue repair and remodeling is thought to be dysregulated.

Indexed as

fibrosisidiopathic pulmonary fibrosislungmast cellsTGF-β

Identifiers

PMID24478701
PMCPMC3896884
OpenAlexW2043695204

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.