Evidence map›Paper›PMID 35789693›Full record

ReviewGefasschirurgie : Zeitschrift fur vaskulare und endovaskulare Chirurgie : Organ der Deutschen und der Osterreichischen Gesellschaft fur Gefasschirurgie unter Mitarbeit der Schweizerischen Gesellschaft fur Gefasschirurgie2022

[Age-related vascular changes exemplified by the carotid artery].

Benedikt Reutersberg, Philip Düppers, Anna-Leonie Menges, Claudia Schrimpf, Alexander Zimmermann, Jaroslav Pelisek

Open access · hybridAbstract readEnglish AbstractReview
In one paragraph

Review in Gefasschirurgie : Zeitschrift fur vaskulare und endovaskulare Chirurgie : Organ der Deutschen und der Osterreichischen Gesellschaft fur Gefasschirurgie unter Mitarbeit der Schweizerischen Gesellschaft fur Gefasschirurgie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. [Open surgical treatment for carotid stenoses].Radiologie (Heidelberg, Germany) · 2024
    Review
  5. Article
  6. Review
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

6 authors at 2 institutions in 1 country.

Benedikt ReutersbergKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
Philip DüppersKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
Anna-Leonie MengesKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
Claudia SchrimpfKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
Alexander ZimmermannKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
Jaroslav PelisekKlinik für Gefäßchirurgie, Universitätsspital Zürich, Rämistr. 100, 8091 Zürich, Schweiz.
University Hospital of Zurich · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the main risk factors for the presence of carotid stenosis and carotid-related stroke is age. The aim of this review article is to present the current state of knowledge on age-related vascular changes using carotid stenosis as an example.Vascular aging (vascular senescence) is a decrease of structural and functional properties of the vessel wall that takes place on different levels. At the multicellular level an increase in vessel volume and diameter as well as intima media thickness occurs with age mainly due to atherosclerotic changes in the vessel wall. At the cellular and extracellular levels there is a decrease in elastin fibers, smooth muscle cells, and total cellularity, an increase in lipid, cholesterol, and calcium phosphate deposition as well as neovascularization. The causes of vascular aging at the molecular level include, in particular oxidative stress, chronic inflammatory response, mitochondrial dysfunction, epigenetic changes, dysregulation of the expression of non-coding RNAs (ncRNAs), and the increase in senescence. Age-related loss of tissue healing and repair capacity make plaques more vulnerable and, in the case of the carotid artery, more susceptible to ischemic stroke.Increasing knowledge of the influence of aging on the epigenetics and ncRNAs in atherosclerotic plaques can in the future more accurately quantify individual patient risk and contribute to the development of targeted therapeutic strategies; however, further studies are needed in this field to understand the full extent of vascular aging and its associated diseases so that these can then be specifically targeted.

Indexed as

AtherosclerosisCarotid stenosisEpigeneticsPlaque morphologyStroke

Identifiers

PMID35789693
PMCPMC9243795
OpenAlexW4283383582

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.