Evidence map›Paper›PMID 35791925›Full record

ArticleJournal of clinical laboratory analysis2022

SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function.

Huiping Gong, Jing Liu, Zhiwei Xue, Wenwen Wang, Cuicui Li, Fanfan Xu, Yimeng Du, Xiaona Lyu

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
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  7. Review
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  9. Exosomal miR-155-5p promote the occurrence of carotid atherosclerosis.Journal of cellular and molecular medicine · 2024
    Article
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  12. Article
  13. Article
  14. Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis.International journal of molecular sciences · 2022
    Review
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  16. 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.

Huiping GongDepartment of Emergency, The Second Hospital of Shandong University, Jinan, China.ORCID https://orcid.org/0000-0002-8221-9318
Jing LiuDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, China.
Zhiwei XueCheeloo College of Medicine, Shandong University, Jinan, China.
Wenwen WangDepartment of Emergency, The Second Hospital of Shandong University, Jinan, China.
Cuicui LiDepartment of Emergency, The Second Hospital of Shandong University, Jinan, China.
Fanfan XuDepartment of Emergency, The Second Hospital of Shandong University, Jinan, China.
Yimeng DuDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, China.
Xiaona LyuDepartment of Pediatric Surgery, Qilu Hospital of Shandong University, Jinan, China.
Second Hospital of Shandong University · CNQilu Hospital of Shandong University · CNShandong University · CN

Funding

Department of Science and Technology of Shandong Province 2017G006029
6 · The paper itself

Abstract

backgroundThis study aimed to explore the relationship between the Sirtuin 3 (SIRT3) gene and endothelial cell dysfunction, contributing to the progression of coronary atherosclerosis driven by hyperglycemia.

methodsWe measured serum SIRT3 levels using enzyme-linked immunosorbent assay in 95 patients with type 2 diabetes mellitus (T2DM) who underwent diagnostic coronary angiography. The patients were divided into two groups according to the presence (n = 45) or absence (n = 50) of coronary artery disease (CAD). Human aortic endothelial cells (HAECs) grown in vitro in a medium with various concentrations of glucose (5.5, 11, 16.5, 22, 27.5, 33, and 38.5 mM) for 24 h were assessed for protein expression of SIRT3, peroxisome proliferator-activated receptor alpha (PPAR-α), endothelial nitric oxide (NO) synthase (eNOS), and inducible NO synthase (iNOS) using Western blot analysis. HAECs were subjected to SIRT3 overexpression or inhibition through SIRT3 adenovirus and siRNA transfection.

resultsSerum SIRT3 levels were significantly lower in T2DM patients with CAD than in those without CAD (p = 0.048). The in vitro results showed that HG significantly increased SIRT3, PPAR-α, and eNOS protein expression in a concentration-dependent manner. Moreover, iNOS expression was decreased in HAECs in response to HG. Reduced PPAR-α and eNOS levels and increased iNOS levels were observed in SIRT3 silenced HAECs cells. In contrast, SIRT3 overexpression significantly improved PPAR-α and eNOS expression and suppressed iNOS expression.

conclusionSIRT3 was associated with the progression of atherosclerosis in T2DM patients through upregulation of PPAR-α and eNOS and downregulation of iNOS, which are involved in endothelial dysfunction under hyperglycemic conditions.

Indexed as

Coronary Artery DiseaseDiabetes Mellitus, Type 2HyperglycemiaSirtuin 3Endothelial CellsHumansNitric Oxide Synthase Type IIIPeroxisome Proliferator-Activated ReceptorsNitric Oxide Synthase Type IIIPeroxisome Proliferator-Activated ReceptorsSIRT3 protein, humanSirtuin 3atherosclerosiscoronary artery diseasediabetesendothelial dysfunctionSirtuin 3

Identifiers

PMID35791925
PMCPMC9396194
OpenAlexW4283831679

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.