Evidence map›Paper›PMID 40180658›Full record

ReviewInnere Medizin (Heidelberg, Germany)2025

[Pathophysiology of fibrosis: inflammatory vs. non-inflammatory].

Elena Neumann, Philipp Klemm

Abstract readEnglish AbstractReview
PubMed Publisher
In one paragraph

Review in Innere Medizin (Heidelberg, Germany), 2025. 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

2 authors.

Elena NeumannAbteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland. e.neumann@kerckhoff-klinik.de.
Philipp KlemmAbteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Justus-Liebig-Universität Gießen, Benekestr. 2-8, 61231, Bad Nauheim, Deutschland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is characterized by an excessive accumulation of extracellular matrix components produced by connective tissue cells. It is a pathophysiological feature of many chronic inflammatory diseases. Nearly every tissue of the body can be affected by fibrosis. Its progression can lead to dysfunction of the affected tissue and organs and potentially death. Early fibrotic mechanisms include the activation of immune responses leading to activation of connective tissue cells and misdirected wound healing responses, finally leading to scarring and fibrosis. Different pathways and factors contribute to the pathophysiology of fibrosis and are summarized in this review.

Indexed as

FibrosisInflammationExtracellular MatrixHumansWound HealingFibroblastsInflammationMyofibroblastsTransforming growth factor betaWound healing

Identifiers

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.