Evidence map›Paper›PMID 29987251›Full record

ReviewInternational journal of molecular sciences2018

Senescent Microvesicles: A Novel Advance in Molecular Mechanisms of Atherosclerotic Calcification.

Matilde Alique, Rafael Ramírez-Carracedo, Guillermo Bodega, Julia Carracedo, Rafael Ramírez

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Extracellular Vesicles as "Very Important Particles" (VIPs) in Aging.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Premature Aging in Chronic Kidney Disease: The Outcome of Persistent Inflammation beyond the Bounds.International journal of environmental research and public health · 2021
    Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020
    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

5 authors at 2 institutions in 1 country.

Matilde AliqueBiology Systems Department, Physiology, Alcala University, Alcala de Henares, 28805 Madrid, Spain. matilde.alique@uah.es.ORCID 0000-0002-7912-1133
Rafael Ramírez-CarracedoCardiovascular Joint Research Unit, University Francisco de Vitoria/University Hospital Ramon y Cajal Research Unit (IRYCIS), 28223 Madrid, Spain. rrcarracedo@hotmail.com.ORCID 0000-0002-8391-2245
Guillermo BodegaBiomedicine and Biotechnology Department, Alcala University, Alcala de Henares, 28805 Madrid, Spain. guillermo.bodega@uah.es.
Julia CarracedoDepartment of Genetic, Physiology and Microbiology, Faculty of Biology, Complutense University/Instituto de Investigación Sanitaria Hospital 12 de Octubre (i+12), 28040 Madrid, Spain. julcar01@ucm.es.ORCID 0000-0002-8422-812X
Rafael RamírezBiology Systems Department, Physiology, Alcala University, Alcala de Henares, 28805 Madrid, Spain. manuel.ramirez@uah.es.ORCID 0000-0003-4598-339X
Universidad de Alcalá · ESUniversidad Francisco de Vitoria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis, a chronic inflammatory disease that causes the most heart attacks and strokes in humans, is the leading cause of death in the developing world; its principal clinical manifestation is coronary artery disease. The development of atherosclerosis is attributed to the aging process itself (biological aging) and is also associated with the development of chronic diseases (premature aging). Both aging processes produce an increase in risk factors such as oxidative stress, endothelial dysfunction and proinflammatory cytokines (oxi-inflamm-aging) that might generate endothelial senescence associated with damage in the vascular system. Cellular senescence increases microvesicle release as carriers of molecular information, which contributes to the development and calcification of atherosclerotic plaque, as a final step in advanced atherosclerotic plaque formation. Consequently, this review aims to summarize the information gleaned to date from studies investigating how the senescent extracellular vesicles, by delivering biological signalling, contribute to atherosclerotic calcification.

Indexed as

AgingAnimalsCell-Derived MicroparticlesCellular SenescenceGenetic Predisposition to DiseaseHumansPlaque, AtheroscleroticRisk FactorsVascular Calcificationagingatherosclerosisendothelial senescencemicrovesiclessenescencevascular calcification

Identifiers

PMID29987251
PMCPMC6073566
OpenAlexW2881915929

What Socratic 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 Socratic graph.