Evidence map›Paper›PMID 24603375›Full record

ReviewDigestive diseases (Basel, Switzerland)2014

Remodeling and fibrosis in chronic eosinophil inflammation.

Seema S Aceves

Abstract readReview
In one paragraph

Review in Digestive diseases (Basel, Switzerland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
6.5field-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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Immune functions of the esophagus.The Journal of allergy and clinical immunology · 2026
    Review
  6. Article
  7. Article
  8. PIEZO1 in Immune Cells: From Force to Function.Results and problems in cell differentiation · 2026
    Review
  9. Article
  10. Review
  11. The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Amphiregulin-producing TThe journal of allergy and clinical immunology. Global · 2024
    Article
  18. Review
  19. Article
  20. Article

3 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

1 author at 1 institution in 1 country.

Seema S AcevesDivision of Allergy, Immunology, Department of Pediatrics and Medicine, University of California, San Diego, Rady Children's Hospital, San Diego, Calif., USA.
Rady Children's Hospital-San Diego · US

Funding

Mechanisms of tissue damage leading to chronic allergic eosinophilic esophagitisR01AI092135 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ACEVES, SEEMA S · 2011 to 2020
$4.4M
NIAID NIH HHS AI092135NIAID NIH HHS R01 AI092135
6 · The paper itself

Abstract

Chronic eosinophilic inflammation has been associated with tissue remodeling in a number of disease states including the hypereosinophilic syndrome (HES), asthma, and, more recently, eosinophilic esophagitis (EoE). Remodeling occurs in the epithelial and subepithelial esophageal tissue, and includes basal zone hyperplasia, epithelial mesenchymal transition, fibrosis, angiogenesis, and smooth muscle hypertrophy/hyperplasia. Previously, research on the clinical impacts of tissue remodeling has been limited by a paucity of human tissue. However, in EoE, recurrent biopsies are required for diagnosis and management. As such, investigators are able to study the associations between tissue changes and clinical disease features. A number of profibrotic and proangiogenic factors are elevated in EoE, including TGF-β1, CCL-18, FGF-9, VEGF, and VCAM-1. Both eosinophils and mast cells produce a number of these factors. TGF-β1 appears to be a master regulator of end-organ dysfunction in EoE and can cause esophageal epithelial mesenchymal transition, fibrosis, and smooth muscle contraction. The requirement for eosinophils, the eosinophilopoietic interleukin, IL-5, and the canonical TGF-β1 signaling pathway for EoE-associated fibrosis, has been invoked using gene-deficient mice. The clinical consequences of eosinophil-associated tissue fibrosis can be devastating, such as endomyocardial fibrosis and heart failure in HES. In EoE, tissue remodeling appears to be the mechanism for multiple cardinal disease complications including esophageal rigidity, strictures, narrowing, and food impactions, as well as the clinical hallmark of dysphagia. Therapies that may be able to reduce or reverse EoE-associated remodeling include topical corticosteroids, anti-IL-5, and food antigen avoidance.

Indexed as

AnimalsEosinophilic EsophagitisEosinophilsEsophagusFibrosisHumansInflammation

Identifiers

PMID24603375
PMCPMC4037288
OpenAlexW2064326663

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.