Evidence map›Paper›PMID 35399949›Full record

ArticleFrontiers in endocrinology2022

Integration of Metabolomics and Proteomics in Exploring the Endothelial Dysfunction Mechanism Induced by Serum Exosomes From Diabetic Retinopathy and Diabetic Nephropathy Patients.

Jing Yang, Dongwei Liu, Zhangsuo Liu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Exosomes applications in kidney diseases.Molecular biology reports · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Research progress on small extracellular vesicles in diabetic nephropathy.Frontiers in cell and developmental biology · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Molecular Pathways of Diabetic Kidney Disease Inferred from Proteomics.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Review
  12. Article
  13. Article
  14. 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

3 authors at 2 institutions in 1 country.

Jing YangDepartment of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Dongwei LiuResearch Institute of Nephrology, Zhengzhou University, Zhengzhou, China.
Zhangsuo LiuResearch Institute of Nephrology, Zhengzhou University, Zhengzhou, China.
Henan Provincial Center for Disease Control and Prevention · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The prevalence of diabetic microvascular diseases has increased significantly worldwide, the most common of which are diabetic nephropathy (DN) and diabetic retinopathy (DR). Microvascular endothelial cells are thought to be major targets of hyperglycemic damage, while the underlying mechanism of diffuse endothelial dysfunction in multiple organs needs to be further investigated. Aim: The aim of this study is to explore the endothelial dysfunction mechanisms of serum exosomes (SExos) extracted from DR and DN (DRDN) patients. Methods: In this study, human glomerular endothelial cells (HGECs) were used as the cell model. Metabolomics ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and proteomics tandem mass tag (TMT)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) together with bioinformatics, the correlation analysis, and the joint pathway analysis were employed to discover the underlying mechanisms of endothelial dysfunction caused by patient's SExos. Results: It can be assumed that serum exosomes extracted by DRDN patients might cause endothelial dysfunction mainly by upregulating alpha subunit of the coagulation factor fibrinogen (FIBA) and downregulating 1-methylhistidine (1-MH). Bioinformatics analysis pointed to an important role in reducing excess cysteine and methionine metabolism. Conclusion: FIBA overexpression and 1-MH loss may be linked to the pathogenicity of diabetic endothelial dysfunction in DR/DN, implying that a cohort study is needed to further investigate the role of FIBA and 1-MH in the development of DN and DR, as well as the related pathways between the two proteins.

Indexed as

Diabetes MellitusDiabetic NephropathiesDiabetic RetinopathyExosomesChromatography, LiquidEndothelial CellsHumansMetabolomicsProteomicsTandem Mass Spectrometrydiabetic nephropathydiabetic retinopathyendothelial dysfunctionexosomesmetabolomicsproteomics

Identifiers

PMID35399949
PMCPMC8991685
OpenAlexW4226244879

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.