Evidence map›Paper›PMID 37960332›Full record

ArticleNutrients2023

Aqueous Fraction from

Celeste Trejo-Moreno, Zimri Aziel Alvarado-Ojeda, Marisol Méndez-Martínez, Mario Ernesto Cruz-Muñoz, Gabriela Castro-Martínez, Gerardo Arrellín-Rosas, Alejandro Zamilpa, Jesús Enrique Jimenez-Ferrer, Juan Carlos Baez Reyes, Gladis Fragoso and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

11 authors at 5 institutions in 1 country.

Celeste Trejo-MorenoFacultad de Medicina, Universidad Autónoma del Estado de Morelos, Cuernavaca 62350, Morelos, Mexico.ORCID 0000-0001-9691-3522
Zimri Aziel Alvarado-OjedaFacultad de Medicina, Universidad Autónoma del Estado de Morelos, Cuernavaca 62350, Morelos, Mexico.
Marisol Méndez-MartínezDepartamento de Sistemas Biológicos, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Xochimilco, Ciudad de México 04960, Mexico.
Mario Ernesto Cruz-MuñozFacultad de Medicina, Universidad Autónoma del Estado de Morelos, Cuernavaca 62350, Morelos, Mexico.
Gabriela Castro-MartínezDoctorado en Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana, Ciudad de México 04960, Mexico.ORCID 0009-0001-0508-486X
Gerardo Arrellín-RosasFacultad de Medicina, Universidad Autónoma del Estado de Morelos, Cuernavaca 62350, Morelos, Mexico.
Alejandro ZamilpaCentro de Investigación Biomédica del Sur, Instituto Mexicano del Seguro Social, Xochitepec 62790, Morelos, Mexico.ORCID 0000-0002-2233-5958
Jesús Enrique Jimenez-FerrerCentro de Investigación Biomédica del Sur, Instituto Mexicano del Seguro Social, Xochitepec 62790, Morelos, Mexico.ORCID 0000-0002-0783-8274
Juan Carlos Baez ReyesEscuela Nacional Preparatoria No. 1, Universidad Nacional Autónoma de México, Ciudad de México 16030, Mexico.
Gladis FragosoInstituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México 04510, Mexico.ORCID 0000-0003-3885-1858
Gabriela Rosas SalgadoFacultad de Medicina, Universidad Autónoma del Estado de Morelos, Cuernavaca 62350, Morelos, Mexico.
Universidad Autónoma del Estado de Morelos · MXMexican Social Security Institute · MXUniversidad Autónoma Metropolitana · MXUniversidad Nacional Autónoma de México · MXUniversidad Panamericana · MX

Funding

Consejo Nacional de Humanidades, Ciencias y Tecnologías CB 2012-169011
6 · The paper itself

Abstract

backgroundEndothelial dysfunction (ED) is a marker of vascular damage and a precursor of cardiovascular diseases such as hypertension, which involve inflammation and organ damage. Nitric oxide (NO), produced by eNOS, which is induced by pAKT, plays a crucial role in the function of a healthy endothelium.

methodsA combination of subfractions SF1 and SF3 (C4) of the aqueous fraction from

resultsCs-AqC4 decreased systolic and diastolic BP, reversed vascular remodeling, decreased IL-1β and TGF-β, increased IL-10, and decreased kidney and liver damage. In HMEC-1 cells, AKT phosphorylation and NO production were increased.

conclusionsCs-AqC4 controlled inflammation and vascular remodeling, alleviating hypertension; it also improved tissue damage associated with ED, probably via Akt activation.

Indexed as

Cucumis sativusHypertensionPeptide HormonesAngiotensin IIAnimalsBlood PressureInflammationMiceMice, Inbred C57BLPlant Components, AerialProto-Oncogene Proteins c-aktVascular RemodelingAngiotensin IIPeptide HormonesProto-Oncogene Proteins c-aktangiotensin-IICucumis sativusendothelial dysfunctionhypertensionmicepAkt

Identifiers

PMID37960332
PMCPMC10649625
OpenAlexW4388333689

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.