Evidence map›Paper›PMID 35207703›Full record

ReviewJournal of personalized medicine2022

Endothelial Senescence and the Chronic Vascular Diseases: Challenges and Therapeutic Opportunities in Atherosclerosis.

Rafael Ramírez, Noemi Ceprian, Andrea Figuer, Gemma Valera, Guillermo Bodega, Matilde Alique, Julia Carracedo

Open access · goldAbstract readReview
In one paragraph

Review in Journal of personalized medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 22 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

7 authors at 2 institutions in 1 country.

Rafael RamírezDepartamento de Biología de Sistemas, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain/Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0003-4598-339X
Noemi CeprianDepartamento de Genética, Fisiología y Microbiología, Facultad de Ciencias Biológicas, Universidad Complutense de Madrid/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28040 Madrid, Spain.ORCID 0000-0001-7028-3083
Andrea FiguerDepartamento de Biología de Sistemas, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain/Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0001-9788-0136
Gemma ValeraDepartamento de Genética, Fisiología y Microbiología, Facultad de Ciencias Biológicas, Universidad Complutense de Madrid/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28040 Madrid, Spain.
Guillermo BodegaDepartamento de Biomedicina y Biotecnología, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain.ORCID 0000-0003-1469-3242
Matilde AliqueDepartamento de Biología de Sistemas, Universidad de Alcalá, 28871 Alcalá de Henares, Madrid, Spain/Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-7912-1133
Julia CarracedoDepartamento de Genética, Fisiología y Microbiología, Facultad de Ciencias Biológicas, Universidad Complutense de Madrid/Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), 28040 Madrid, Spain.ORCID 0000-0002-8422-812X
Universidad de Alcalá · ESUniversidad Complutense de Madrid · ES

Funding

Instituto de Salud Carlos III PI17/01029Instituto de Salud Carlos III PI19/00240Instituto de Salud Carlos III PI20/01321
6 · The paper itself

Abstract

Atherosclerosis is probably one of the paradigms of disease linked to aging. Underlying the physiopathology of atherosclerosis are cellular senescence, oxidative stress, and inflammation. These factors are increased in the elderly and from chronic disease patients. Elevated levels of oxidative stress affect cellular function and metabolism, inducing senescence. This senescence modifies the cell phenotype into a senescent secretory phenotype. This phenotype activates immune cells, leading to chronic systemic inflammation. Moreover, due to their secretory phenotype, senescence cells present an increased release of highlighted extracellular vesicles that will change nearby/neighborhood cells and paracrine signaling. For this reason, searching for specific senescent cell biomarkers and therapies against the development/killing of senescent cells has become relevant. Recently, senomorphic and senolityc drugs have become relevant in slowing down or eliminating senescence cells. However, even though they have shown promising results in experimental studies, their clinical use is still yet to be determined.

Indexed as

atherosclerosiscellular senescenceendothelial senescenceextracellular vesiclesinflammationsenolityc

Identifiers

PMID35207703
PMCPMC8874678
OpenAlexW4210637844

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.