Evidence map›Paper›PMID 36555139›Full record

ArticleInternational journal of molecular sciences2022

Impacts of Telomeric Length, Chronic Hypoxia, Senescence, and Senescence-Associated Secretory Phenotype on the Development of Thoracic Aortic Aneurysm.

Thomas Aschacher, Daniela Geisler, Verena Lenz, Olivia Aschacher, Bernhard Winkler, Anne-Kristin Schaefer, Andreas Mitterbauer, Brigitte Wolf, Florian K Enzmann, Barbara Messner and 4 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

14 authors at 4 institutions in 1 country.

Thomas AschacherDepartment of Cardiovascular Surgery, Clinic Floridsdorf and Karl Landsteiner Institute for Cardio-Vascular Research, 1210 Vienna, Austria.ORCID 0000-0003-3373-8194
Daniela GeislerDepartment of Cardiovascular Surgery, Clinic Floridsdorf and Karl Landsteiner Institute for Cardio-Vascular Research, 1210 Vienna, Austria.
Verena LenzDepartment of Cardiovascular Surgery, Clinic Floridsdorf and Karl Landsteiner Institute for Cardio-Vascular Research, 1210 Vienna, Austria.
Olivia AschacherDepartment of Plastic, Reconstructive and Aesthetic Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Bernhard WinklerDepartment of Cardiovascular Surgery, Clinic Floridsdorf and Karl Landsteiner Institute for Cardio-Vascular Research, 1210 Vienna, Austria.
Anne-Kristin SchaeferDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0002-9268-2461
Andreas MitterbauerDepartment of General Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Brigitte WolfDepartment of General Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Florian K EnzmannDepartment of Vascular Surgery, Medical University of Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0002-7200-4145
Barbara MessnerDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-8331-6497
Günther LauferDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-7257-110X
Marek P EhrlichDepartment of Cardiac Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Martin GrabenwögerDepartment of Cardiovascular Surgery, Clinic Floridsdorf and Karl Landsteiner Institute for Cardio-Vascular Research, 1210 Vienna, Austria.
Michael BergmannDepartment of General Surgery, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0001-8529-1166
Medical University of Vienna · ATKarl Landsteiner Society · ATSigmund Freud Privatuniversität Wien · ATInnsbruck Medical University · AT

Funding

Medical-Scientific Fund of the Mayor of Vienna, grant number AP15115
6 · The paper itself

Abstract

Thoracic aortic aneurysm (TAA) is an age-related and life-threatening vascular disease. Telomere shortening is a predictor of age-related diseases, and its progression is associated with premature vascular disease. The aim of the present work was to investigate the impacts of chronic hypoxia and telomeric DNA damage on cellular homeostasis and vascular degeneration of TAA. We analyzed healthy and aortic aneurysm specimens (215 samples) for telomere length (TL), chronic DNA damage, and resulting changes in cellular homeostasis, focusing on senescence and apoptosis. Compared with healthy thoracic aorta (HTA), patients with tricuspid aortic valve (TAV) showed telomere shortening with increasing TAA size, in contrast to genetically predisposed bicuspid aortic valve (BAV). In addition, TL was associated with chronic hypoxia and telomeric DNA damage and with the induction of senescence-associated secretory phenotype (SASP). TAA-TAV specimens showed a significant difference in SASP-marker expression of IL-6, NF-κB, mTOR, and cell-cycle regulators (γH2AX, Rb, p53, p21), compared to HTA and TAA-BAV. Furthermore, we observed an increase in CD163

Indexed as

Aortic Aneurysm, ThoracicBicuspid Aortic Valve DiseaseHeart Valve DiseasesAortic ValveHumansSenescence-Associated Secretory Phenotypeaneurysmcell deathDNA damagesenescence-associated secretory phenotypetelocytestelomerethoracic aorta

Identifiers

PMID36555139
PMCPMC9779024
OpenAlexW4311849773

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.