Evidence map›Paper›PMID 42790271›Full record

ArticleJACC. Basic to translational science2026

Targeting the ERK Signaling Pathway to Halt Adventitia Remodeling of Ascending Thoracic Aortic Aneurysm.

Khaled Ak Mohammed, Elisa Avolio, Valeria V Alvino, Eltayeb Mohamed Ahmed, Cha Rajakaruna, Ahmed Ghoneim, Ahmed Elminshawy, Gianni D Angelini, Paolo Madeddu

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Khaled Ak MohammedBristol Heart Institute, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom; Department of Cardiothoracic Surgery, Faculty of Medicine, Assiut University, Assiut, Egypt; Bristol Heart Institute, Bristol Royal Infirmary, University Hospitals Bristol and Weston NHS Foundation Trust, Bristol, United Kingdom.
Elisa AvolioBristol Heart Institute, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom. Electronic address: elisa.avolio@bristol.ac.uk.
Valeria V AlvinoBristol Heart Institute, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Eltayeb Mohamed AhmedBristol Heart Institute, Bristol Royal Infirmary, University Hospitals Bristol and Weston NHS Foundation Trust, Bristol, United Kingdom.
Cha RajakarunaBristol Heart Institute, Bristol Royal Infirmary, University Hospitals Bristol and Weston NHS Foundation Trust, Bristol, United Kingdom.
Ahmed GhoneimDepartment of Cardiothoracic Surgery, Faculty of Medicine, Assiut University, Assiut, Egypt.
Ahmed ElminshawyDepartment of Cardiothoracic Surgery, Faculty of Medicine, Assiut University, Assiut, Egypt.
Gianni D AngeliniBristol Heart Institute, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom; Bristol Heart Institute, Bristol Royal Infirmary, University Hospitals Bristol and Weston NHS Foundation Trust, Bristol, United Kingdom.
Paolo MadedduBristol Heart Institute, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom. Electronic address: paolo.madeddu@bristol.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ascending thoracic aortic aneurysms (AsTAAs) are life-threatening and lack effective drug treatments. This study investigated whether abnormal mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) activation in adventitial pericytes contributes to aneurysm progression. Human AsTAA tissue showed vasa vasorum remodeling and displaced pericytes. Isolated AsTAA-pericytes showed increased MEK/ERK signaling, proliferation, migration, proteolytic activity, proinflammatory secretome, and altered angiogenic function. These changes were reversed by the MEK inhibitor PD0325901. In a mouse model, short-term MEKi treatment reduced aortic dilatation, improved compliance, preserved elastin, and lessened inflammation, without adverse effects. This is the first study identifying dysregulated adventitial pericytes as a hallmark of AsTAA, supporting MEKi as a promising therapeutic.

Indexed as

aorta adventitiaaorta aneurysm mouse modelaorta pericytesascending thoracic aorta aneurysmMEK inhibitorPD0325901

Identifiers

PMID42790271
PMCPMC13635404

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.