Evidence map›Paper›PMID 34218268›Full record

ArticleJournal of human hypertension2022

Differentially expressed proteins in platelets derived from patients with hypertension.

Yobana Armenta-Medina, Ivette Martínez-Vieyra, Oscar Medina-Contreras, Claudia G Benitez-Cardoza, Albertana Jiménez-Pineda, César A Reyes-López, Doris Cerecedo

Open access · bronzeAbstract read
In one paragraph

Article in Journal of human hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

7 authors at 2 institutions in 1 country.

Yobana Armenta-MedinaLaboratorio de Hematobiología, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico.ORCID 0000-0003-0462-1683
Ivette Martínez-VieyraLaboratorio de Hematobiología, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico.
Oscar Medina-ContrerasUnidad de Investigación Epidemiológica en Endocrinología y Nutrición, Hospital Infantil de México Federico Gómez, Mexico City, Mexico.ORCID 0000-0002-4432-7780
Claudia G Benitez-CardozaLaboratorio de Investigación Bioquímica, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico.
Albertana Jiménez-PinedaLaboratorio de Investigación Bioquímica, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico.ORCID 0000-0001-8047-0325
César A Reyes-LópezLaboratorio de Bioquímica Estructural, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico.ORCID 0000-0002-9860-8983
Doris CerecedoLaboratorio de Hematobiología, ENMyH, Instituto Politécnico Nacional, Mexico City, Mexico. dcereced@ipn.mx.ORCID 0000-0002-0015-8081
Instituto Politécnico Nacional · MXHospital Infantil de México Federico Gómez · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertension (HTN) causes end-organ damage and is a major cause of morbidity and mortality globally. Recent studies suggested blood cells participate in the maintenance of HTN. Platelets-anucleated cell fragments derived from megakaryocytes-exert diverse functions, including their well-characterized role in the formation of hemostatic clots. However, platelets from patients with HTN exhibit altered membrane lipid and protein compositions that impact platelet function and lead to formation of aggregates and vascular obstructions. Here, for the first time, we have identified, by proteomic analyses, the most relevant 11 proteins that show the greatest difference in their expression in platelets derived from patients with HTN, in comparison with those from normotensive individuals. These proteins are involved in cytoskeletal organization and the coagulation cascade that contributes to platelet activation, release of granule contents, and aggregation, which culminate in thrombus formation. These results have important implications in our understanding of the molecular mechanisms associated with the development of HTN, and in consequence, the development of new strategies to counteract the cardiovascular disorders associated with constitutive activation of platelets in HTN.

Indexed as

HypertensionThrombosisBlood PlateletsHumansMegakaryocytesPlatelet ActivationProteomics

Identifiers

PMID34218268
PMCPMC8254060
OpenAlexW3179159338

What OpenQuestion holds

Textmetadata
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.