Evidence map›Paper›PMID 34803387›Full record

ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2021

RPS4Y1 Promotes High Glucose-Induced Endothelial Cell Apoptosis and Inflammation by Activation of the p38 MAPK Signaling.

Yuan Chen, Yiheng Chen, Chonghui Tang, Qian Zhao, Tailin Xu, Qi Kang, Bin Jiang, Li Zhang

Open access · goldAbstract read
In one paragraph

Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. A Novel Regulatory Role for RPS4Y1 in Inflammatory and Fibrotic Processes.International journal of molecular sciences · 2025
    Article
  6. Article
  7. Importance of STAT3 signaling in preeclampsia (Review).International journal of molecular medicine · 2025
    Review
  8. Ribosomal protein paralogues in ribosome specialization.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Suppression of SMOC2 alleviates myocardial fibrosisFrontiers in cardiovascular medicine · 2022
    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

8 authors at 3 institutions in 1 country.

Yuan Chen *Department of Endocrinology, The First People's Hospital of Zunyi, Zunyi, Guizhou, 563000, People's Republic of China.
Yiheng Chen *Department of Hand and Plastic Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.
Chonghui TangDepartment of Neurosurgery, Affiliated Cixi Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 315300, People's Republic of China.
Qian ZhaoDepartment of Endocrinology, The First People's Hospital of Zunyi, Zunyi, Guizhou, 563000, People's Republic of China.
Tailin XuDepartment of Endocrinology, The First People's Hospital of Zunyi, Zunyi, Guizhou, 563000, People's Republic of China.
Qi KangDepartment of Endocrinology, The First People's Hospital of Zunyi, Zunyi, Guizhou, 563000, People's Republic of China.
Bin JiangDepartment of Hand and Plastic Surgery, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, People's Republic of China.
Li ZhangDepartment of Neurosurgery, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China.
First People’s Hospital of Zunyi · CNWenzhou Medical University · CNChina-Japan Friendship Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimEndothelial dysfunction is a key pathological basis for diabetes mellitus complications, including diabetic nephropathy, diabetic retinopathy, and diabetic cardiomyopathy. This study aimed to reveal the functional role of ribosomal protein S4 Y-linked 1 (RPS4Y1) in endothelial dysfunction.

methodsHuman umbilical vein endothelial cells (HUVECs) were subjected to high glucose. The expression of RPS4Y1 in cells was overexpressed or silenced by plasmid or siRNA transfection. MTT assay, flow cytometry, JC-1 probe, scratch test, tube formation, and ELISA were conducted to assess the effects of RPS4Y1 on cell. Western blot was performed to assay the downstream signaling of RPS4Y1. The inhibitors of p38, ERK, and Jnk were used to treat cells to validate the involvement of them in RPS4Y1-mediated endothelial dysfunction.

resultsRPS4Y1 was upregulated in HUVECs in response to high glucose in both dose- and time-dependent manners. Overexpression of RPS4Y1 induced viability loss, apoptosis, and inflammation, but inhibited cell migration and tube formation. Silence of RPS4Y1 impacted these aspects in a contrary trend. The phosphorylation of p38 rather than ERK and Jnk was activated by RPS4Y1. In addition, the dysfunction of HUVECs mediated by RPS4Y1 was attenuated by SB203580 (a specific inhibitor of p38 signaling).

conclusionThe highly expressed RPS4Y1 in endothelial cells may contribute to high glucose-induced dysfunction through regulating p38 MAPK signaling. RPS4Y1 might be a potential therapeutic target for treating diabetes mellitus complications.

Indexed as

diabetes mellitushigh glucoseHUVECp38 MAPK signalingRPS4Y1

Identifiers

PMID34803387
PMCPMC8594791
OpenAlexW3214544219

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Registered trials

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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.