Evidence map›Paper›PMID 38356516›Full record

ArticleHeliyon2024

Systematic review and bioinformatics analysis of plasma and serum extracellular vesicles proteome in type 2 diabetes.

Jeanette Guadalupe Arredondo-Damián, Juan Manuel Martínez-Soto, Francisco A Molina-Pelayo, Jesús Adriana Soto-Guzmán, Luis Castro-Sánchez, Luis Fernando López-Soto, Maria Del Carmen Candia-Plata

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Improvement of small extracellular vesicle isolation from mouse model blood.Extracellular vesicles and circulating nucleic acids · 2025
    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

7 authors at 2 institutions in 1 country.

Jeanette Guadalupe Arredondo-DamiánDoctoral Program in Sciences (Chemical-Biological and Health), University of Sonora, Hermosillo, Sonora, Mexico.
Juan Manuel Martínez-SotoDepartment of Medicine and Health Sciences, University of Sonora, Hermosillo, Sonora, Mexico.
Francisco A Molina-PelayoUniversity Center for Biomedical Research, University of Colima, Colima, Colima, Mexico.
Jesús Adriana Soto-GuzmánDepartment of Medicine and Health Sciences, University of Sonora, Hermosillo, Sonora, Mexico.
Luis Castro-SánchezUniversity Center for Biomedical Research, University of Colima, Colima, Colima, Mexico.
Luis Fernando López-SotoDepartment of Medicine and Health Sciences, University of Sonora, Hermosillo, Sonora, Mexico.
Maria Del Carmen Candia-PlataDepartment of Medicine and Health Sciences, University of Sonora, Hermosillo, Sonora, Mexico.
Universidad de Sonora · MXUniversidad de Colima · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Type 2 diabetes (T2D) is a complex metabolic ailment marked by a global high prevalence and significant attention in primary healthcare settings due to its elevated morbidity and mortality rates. The pathophysiological mechanisms underlying the onset and progression of this disease remain subjects of ongoing investigation. Recent evidence underscores the pivotal role of the intricate intercellular communication network, wherein cell-derived vesicles, commonly referred to as extracellular vesicles (EVs), emerge as dynamic regulators of diabetes-related complications. Given that the protein cargo carried by EVs is contingent upon the metabolic conditions of the originating cells, particular proteins may serve as informative indicators for the risk of activating or inhibiting signaling pathways crucial to the progression of T2D complications. Methods: In this study, we conducted a systematic review to analyze the published evidence on the proteome of EVs from the plasma or serum of patients with T2D, both with and without complications (PROSPERO: CRD42023431464). Results: Nine eligible articles were systematically identified from the databases, and the proteins featured in these articles underwent Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. We identified changes in the level of 426 proteins, with CST6, CD55, HBA1, S100A8, and S100A9 reported to have high levels, while FGL1 exhibited low levels. Conclusion: These proteins are implicated in pathophysiological mechanisms such as inflammation, complement, and platelet activation, suggesting their potential as risk markers for T2D development and progression. Further studies are required to explore this topic in greater detail.

Indexed as

ComplementEVExtracellular vesiclesInflammationPlatelet activationProteomeSystematic reviewT2DType 2 diabetes

Identifiers

PMID38356516
PMCPMC10865249
OpenAlexW4391540699

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.