Evidence map›Paper›PMID 42670708›Full record

ReviewClinical transplantation2026

What Explains the Pattern of Fibrosis in Chronic Graft-Versus-Host Disease?

Mohammadamin Noorafrooz, Hoda Kavosi, Robert Peter Gale

Abstract readReview
In one paragraph

Review in Clinical transplantation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Mohammadamin NoorafroozVali-E-Asr Reproductive Health Research Center, Family Health Research Institute, Tehran University of Medical Sciences, Tehran, Iran.
Hoda KavosiRheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Robert Peter GaleCentre For Haematology, Department of Immunology and Inflammation, Imperial College of Science, Technology and Medicine, London, UK.

Funding

National Institute of Health Research (NIHR) Biomedical Research Centre
6 · The paper itself

Abstract

Fibrosis is common in diverse conditions but has different patterns across tissues and organs despite shared cellular and molecular pathways reasons for which are mostly unexplained. In this review we discuss chronic graft-Versus-host disease (GvHD), progressive systemic sclerosis (PSS), idiopathic pulmonary fibrosis (IPF), primary myelofibrosis (PMF), chronic lung allograft dysfunction (CLAD) and VEXAS syndrome to explore potential mechanisms underlying these patterns of fibrosis. We propose the distribution of fibrosis reflects a complex interplay between aetiology, initiating stimuli, local immune response, tissue-specific micro-environment and host susceptibility. Distinguishing systemic and local drivers of fibrosis is needed to understand and explain these patterns. A deeper understanding of early, tissue-specific events governing fibrotic responses may allow development of preventive and therapeutic strategies.

Indexed as

FibrosisGraft vs Host DiseaseIdiopathic Pulmonary FibrosisPrimary MyelofibrosisChronic DiseaseHumansPrognosisScleroderma, SystemicChronic graft‐Versus‐host diseasechronic lung allograft dysfunctionfibrosisidiopathic pulmonary fibrosisprimary myelofibrosisprogressive systemic sclerosisVEXAS

Identifiers

PMID42670708
PMCPMC13527652

What OpenQuestion 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 OpenQuestion graph.