Evidence map›Paper›PMID 42350581›Full record

ArticleScientific reports2026

Aortic asprosin overexpression does not ameliorate disease pathophysiology in a murine model of Marfan syndrome.

Prithviraj Manohar Vijaya Shetty, Andrea Matzen, Susanne Hille, Sabine Michalewski, Henrike Witthaus, Marie Noormalal, Fady Marcous, Yousef Morcos, Tarik Bozoglu, Wiebke Sommer and 8 more

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In one paragraph

Article in Scientific reports, 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

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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

18 authors.

Prithviraj Manohar Vijaya ShettyDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
Andrea MatzenDepartment of Animal Welfare, CAU Kiel, Kiel, Germany.
Susanne HilleDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
Sabine MichalewskiDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
Henrike WitthausDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany.
Marie NoormalalDepartment of Internal Medicine III, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Kiel, Germany.
Fady MarcousDepartment of Pediatrics and Adolescent Medicine, Faculty of Medicine, University Hospital Cologne, University of Cologne, Cologne, Germany.
Yousef MorcosDepartment of Pediatrics and Adolescent Medicine, Faculty of Medicine, University Hospital Cologne, University of Cologne, Cologne, Germany.
Tarik BozogluKlinik und Poliklinik für Innere Medizin I, University Clinic rechts der Isar, Technical University Munich, Munich, Germany.
Wiebke SommerDepartment of Cardiac Surgery, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Kiel, Germany.
Gregor WarneckeDepartment of Cardiac Surgery, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Kiel, Germany.
Christian KupattKlinik und Poliklinik für Innere Medizin I, University Clinic rechts der Isar, Technical University Munich, Munich, Germany.
Andreas H WagnerDepartment of Cardiovascular Physiology, Heidelberg University, Heidelberg, Germany.
Regina ScherließDepartment of Pharmaceutics and Biopharmaceutics, Kiel University, Kiel, Germany.
Derk FrankDepartment of Internal Medicine III, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Kiel, Germany.
Gerhard SengleDepartment of Pediatrics and Adolescent Medicine, Faculty of Medicine, University Hospital Cologne, University of Cologne, Cologne, Germany.
Oliver J MüllerDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany. oliver.mueller@uksh.de.
Anca Kliesow RemesDepartment of Internal Medicine V, University Hospital Schleswig-Holstein, University of Kiel, German Centre for Cardiovascular Research (DZHK), Partner Site North, Arnold-Heller-Str. 3, 24105, Kiel, Germany. anca.remes@uksh.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Marfan syndrome (MFS) is a connective tissue disorder caused by FBN1 mutations, characterised by aortic aneurysms leading to life-threatening dissections. Asprosin is the C-terminal propeptide of fibrillin-1 that was shown to function as a glucogenic hormone with critical implications in vascular pathology. However, its role in MFS remains unknown. Here, we investigate the effect of asprosin overexpression in vascular smooth muscle cells (VSMCs) and in the Marfan mouse model mgR/mgR via endothelial-targeted transduction by adeno-associated viruses (AAVs). In both human and murine VSMCs, asprosin overexpression did not alter VCAM1 or MMP9 expression, while TNF-α-stimulated asprosin-overexpressing MOVAS cells exhibited reduced IL6 levels. In mgR/mgR mice, asprosin overexpression did not affect aortic diameter or elastin integrity. Molecular analyses revealed no significant change in inflammatory or epithelial-to-mesenchymal transition (EMT) markers at the mRNA or protein level, with VCAM1 and MMP9 remaining unchanged. Together, these findings indicate that asprosin overexpression does not ameliorate the aneurysmal phenotype in MFS.

Indexed as

AortaFibrillin-1Marfan SyndromeAdipokinesAnimalsDisease Models, AnimalFemaleGene Expression RegulationHumansMaleMatrix Metalloproteinase 9MiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleVascular Cell Adhesion Molecule-1AdipokinesFBN1 protein, humanFbn1 protein, mouseFibrillin-1Matrix Metalloproteinase 9Vascular Cell Adhesion Molecule-1

Identifiers

PMID42350581
PMCPMC13303822

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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.