Evidence map›Paper›PMID 42509396›Full record

ArticleHepatology international2026

Histomorphometry indicates distinct contributions of myofibroblast activation and sinusoidal capillarization to portal hypertension.

Thomas Sorz-Nechay, Benedikt S Hofer, Philipp Königshofer, Alexis Treitler, Georg Semmler, Benedikt Simbrunner, Vlad Taru, Katharina Bonitz, Henriette Horstmeier, Georg Kramer and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Hepatology international, 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

20 authors.

Thomas Sorz-NechayDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Benedikt S HoferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Philipp KönigshoferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Alexis TreitlerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Georg SemmlerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Benedikt SimbrunnerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Vlad TaruDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Katharina BonitzDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Henriette HorstmeierDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Georg KramerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Kerstin ZinoberDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Katharina RegnatDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Barbara NeudertDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Christopher C KalteneckerDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Behrang MozayaniDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Renate KainDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Michael TraunerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Mattias MandorferDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Philipp SchwablDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria.
Thomas ReibergerDivision of Gastroenterology and Hepatology, Department of Medicine III, Medical University of Vienna, Währinger Guertel 18-20, 1090, Vienna, Austria. thomas.reiberger@meduniwien.ac.at.ORCID http://orcid.org/0000-0002-4590-3583

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsPortal hypertension (PH) is a severe consequence of cirrhosis and the primary driver of hepatic decompensation. We aimed to investigate the link between histological myofibroblast activation (alpha-smooth-muscle-actin: αSMA) and sinusoidal capillarization (CD34) markers to PH severity in patients with chronic liver disease (CLD).

methodsPatients with CLD underwent hepatic venous pressure gradient (HVPG) measurement and liver biopsy. Liver samples were stained by picrosirius-red for collagen proportionate area (CPA) and for αSMA/CD34. Quantitative histomorphometry was performed on full-slide scans.

results102 patients (63.7% male, median age 56.4 years, mainly steatotic liver disease: 58.8%) were included. The median HVPG was 13 [10-18] mmHg and severe PH (HVPG ≥ 16 mmHg, PH16) was found in 35.3%. Median liver-stiffness was 30.6 [19.1-57.6] kPa. In PH16 patients, fibrosis (CPA: 28.39 vs 17.72%), myofibroblast activation (αSMA: 10.84 vs 3.75%), and capillarization (CD34: 5.45 vs 2.67%) were significantly more pronounced (all p < 0.001 vs. no PH16). CD34 showed a higher correlation to HVPG (rho = 0.505) than CPA (rho = 0.472) and αSMA (rho = 0.347, all p < 0.001). CD34 expression was independently correlated with enhanced liver fibrosis (ELF) test and von Willebrand factor (VWF). When partially adjusting for fibrosis severity, patients with less severe fibrosis and high αSMA or CD34 had a trend for higher HVPG, whereas in intermediate fibrosis, only CD34-high patients trended higher HVPG.

conclusionCPA, CD34 and αSMA expression all correlate with PH severity. CD34 represents a histologic sinusoidal capillarization marker that correlates with circulating VWF and ELF. αSMA and CD34 represent potential histologic markers of PH beyond the static component.

Indexed as

BiomarkerChronic liver diseaseCirrhosisHistologyLiver fibrosisPathophysiologyPortal hypertension

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.