Evidence mapPaperPMID 42417160Full record

ReviewJCI insight2026

The inflammatory/fibrotic axis across organs: myelofibrosis as a model of reversibility.

Lucas Greven, Stijn Nr Fuchs, Hélène Fe Gleitz, Rebekka K Schneider

Abstract readReview
In one paragraph

Review in JCI insight, 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

4 authors.

Lucas GrevenInstitute for Cell and Tumor Biology, RWTH Aachen University Hospital, Aachen, Germany.
Stijn Nr FuchsDepartment of Developmental Biology and.
Hélène Fe GleitzInstitute for Cell and Tumor Biology, RWTH Aachen University Hospital, Aachen, Germany.
Rebekka K SchneiderInstitute for Cell and Tumor Biology, RWTH Aachen University Hospital, Aachen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis affects almost all organ systems, resulting in a dysfunctional extracellular matrix that impairs function and can lead to failure. Crosstalk between immune cells and the stromal environment exacerbates fibrosis in all organs and is an attractive therapeutic target. Here, we discuss recent findings regarding the cellular and molecular mechanisms that underlie inflammation and fibrosis across organs. We focus on how reciprocal immune/stromal signaling maintains fibrotic niches, outline strategies for therapeutic intervention beyond current antifibrotic agents, and highlight the bone marrow fibrotic disease myelofibrosis as a model for understanding, and ultimately reversing, fibrosis in human disease.

Indexed as

InflammationPrimary MyelofibrosisAnimalsBone MarrowExtracellular MatrixFibrosisHumansSignal Transduction

Identifiers

PMID42417160
PMCPMC13460818

What Socratic holds

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LicenceCC BY
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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.