Evidence map›Paper›PMID 30671170›Full record

ArticleOxidative medicine and cellular longevity2018

Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome.

Ocarol López-Acosta, María de Los Angeles Fortis-Barrera, Miguel Angel Barrios-Maya, Angélica Ruiz Ramírez, Francisco Javier Alarcón Aguilar, Mohammed El-Hafidi

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  9. Tale of two kinases: Protein kinase A and CaWorld journal of diabetes · 2021
    Review
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  11. Review
  12. Article
  13. Mitochondrial CaJournal of molecular and cellular cardiology · 2021
    Review
  14. Prevention of Fine Dust-Induced Vascular Senescence byAntioxidants (Basel, Switzerland) · 2020
    Article
  15. Article
  16. Article
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  18. 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

6 authors at 2 institutions in 1 country.

Ocarol López-AcostaUniversidad Autónoma Metropolitana Unidad Iztapalapa, Doctorado Ciencias Biológicas y de la Salud, Avenida San Rafael Atlixco 186, Vicentina, Iztapalapa, 09340 Ciudad de México, Mexico.
María de Los Angeles Fortis-BarreraUniversidad Autónoma Metropolitana Unidad Iztapalapa, Laboratorio de Farmacología, Departamento de Ciencias de la Salud, Avenida San Rafael Atlixco 186, Vicentina, Iztapalapa, 09340 Ciudad de México, Mexico.
Miguel Angel Barrios-MayaInstituto Nacional de Cardiología Ignacio Chávez, Departamento de Biomedicina Cardiovascular, Juan Badiano No 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, Mexico.
Angélica Ruiz RamírezInstituto Nacional de Cardiología Ignacio Chávez, Departamento de Biomedicina Cardiovascular, Juan Badiano No 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, Mexico.
Francisco Javier Alarcón AguilarUniversidad Autónoma Metropolitana Unidad Iztapalapa, Laboratorio de Farmacología, Departamento de Ciencias de la Salud, Avenida San Rafael Atlixco 186, Vicentina, Iztapalapa, 09340 Ciudad de México, Mexico.
Mohammed El-HafidiInstituto Nacional de Cardiología Ignacio Chávez, Departamento de Biomedicina Cardiovascular, Juan Badiano No 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, Mexico.ORCID 0000-0002-5235-5642
Instituto Nacional de Cardiología · MXUniversidad Autónoma Metropolitana · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In metabolic diseases, the increased reactive oxygen species (ROS) represents one of the pathogenic mechanisms for vascular disease probably by promoting vascular smooth muscle cell (SMC) proliferation that contributes to the development of arterial remodeling and stenosis, hypertension, and atherosclerosis. Therefore, this work was undertaken to evaluate the participation of ROS from NADPH oxidase and mitochondria in the proliferation of SMCs from the aorta in a model of metabolic syndrome induced by sucrose feeding in rats. After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. In addition SMCs from SF rats had a higher growth rate and produce more ROS than control cells. The treatment of SMCs with DPI and apocynin to inhibit NADPH oxidase and with tempol to scavenge superoxide anion significantly blocked the proliferation of both SF and control cells suggesting the participation of NADPH oxidase as a source of superoxide anion. MitoTEMPO, which targets mitochondria within the cell, also significantly inhibited the proliferation of SMCs having a greater effect on cells from SF than from the control aorta. The higher rate of cell growth from the SF aorta is supported by the increased content of cyclophilin A and CD147, proteins involved in the mechanism of cell proliferation. In addition, caldesmon,

Indexed as

Cell ProliferationAnimalsAortaDisease Models, AnimalMaleMetabolic SyndromeMitochondria, MuscleMuscle, Smooth, VascularMyocytes, Smooth MuscleNADPH OxidasesRatsRats, WistarReactive Oxygen SpeciesNADPH OxidasesReactive Oxygen Species

Identifiers

PMID30671170
PMCPMC6323422
OpenAlexW2905735996

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.