Evidence map›Paper›PMID 32083977›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2020

Pathogenic mechanisms and the potential of drug therapies for aortic aneurysm.

Bo Liu, David J Granville, Jonathan Golledge, Zamaneh Kassiri

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% of its field
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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

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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 at 4 institutions in 3 countries.

Bo LiuUniversity of Wisconsin, Madison, Department of Surgery, Madison Wisconsin.
David J GranvilleInternational Collaboration on Repair Discoveries Centre and University of British Columbia Centre for Heart Lung Innovation, Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada.ORCID 0000-0001-6985-2816
Jonathan GolledgeThe Queensland Research Centre for Peripheral Vascular Disease, College of Medicine and Dentistry, James Cook University, Department of Vascular and Endovascular Surgery, Townsville Hospital and Health Services, Townsville, Queensland, Australia.
Zamaneh KassiriUniversity of Alberta, Department of Physiology, Cardiovascular Research Center, Faculty of Medicine and Dentistry, Edmonton, Alberta, Canada.
Townsville Hospital · AUUniversity of Alberta · CAUniversity of British Columbia · CAUniversity of Wisconsin–Madison · US

Funding

Molecular Mechanisms in Abdominal Aortic AneuysmR01HL088447 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2011 to 2020
$3.8M
Vascular smooth muscle cell apoptosis in intimal hyperplasiaR01HL122562 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2015 to 2018
$1.6M
Canadian Institutes for Health ResearchNHLBI NIH HHS R01 HL088447NHLBI NIH HHS R01 HL122562
6 · The paper itself

Abstract

Aortic aneurysm is a permanent focal dilation of the aorta. It is usually an asymptomatic disease but can lead to sudden death due to aortic rupture. Aortic aneurysm-related mortalities are estimated at ∼200,000 deaths per year worldwide. Because no pharmacological treatment has been found to be effective so far, surgical repair remains the only treatment for aortic aneurysm. Aortic aneurysm results from changes in the aortic wall structure due to loss of smooth muscle cells and degradation of the extracellular matrix and can form in different regions of the aorta. Research over the past decade has identified novel contributors to aneurysm formation and progression. The present review provides an overview of cellular and noncellular factors as well as enzymes that process extracellular matrix and regulate cellular functions (e.g., matrix metalloproteinases, granzymes, and cathepsins) in the context of aneurysm pathogenesis. An update of clinical trials focusing on therapeutic strategies to slow abdominal aortic aneurysm growth and efforts underway to develop effective pharmacological treatments is also provided.

Indexed as

Aortic AneurysmDisease ProgressionExtracellular MatrixHumansMatrix MetalloproteinasesMuscle, Smooth, VascularMyocytes, Smooth MuscleVascular RemodelingMatrix Metalloproteinasesaortic aneurysmaortic remodelingproteasessmooth muscle cells

Identifiers

PMID32083977
PMCPMC7099451
OpenAlexW3008229330

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.