Evidence map›Paper›PMID 29336364›Full record

ArticleChinese medical journal2018

Mechanism of Chronic Stress-induced Reduced Atherosclerotic Medial Area and Increased Plaque Instability in Rabbit Models of Chronic Stress.

Ze-Mou Yu, Xiao-Tao Deng, Ruo-Mei Qi, Lu-Yan Xiao, Chong-Qing Yang, Tao Gong

Open access · goldAbstract read
In one paragraph

Article in Chinese medical journal, 2018. 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
2.2field-weighted citation impact, top 11% 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, 24 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Recent Progress of Chronic Stress in the Development of Atherosclerosis.Oxidative medicine and cellular longevity · 2022
    Review
  9. The "Angiogenic Switch" and Functional Resources in Cyclic Sports Athletes.International journal of molecular sciences · 2021
    Review
  10. Article
  11. VEGF-A in Cardiomyocytes and Heart Diseases.International journal of molecular sciences · 2020
    Review
  12. Review
  13. Cardioprotective Effect of (Cardiovascular therapeutics · 2020
    Article
  14. Chronic stress: a crucial promoter of cell apoptosis in atherosclerosis.The Journal of international medical research · 2020
    Article
  15. Article
  16. 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

6 authors at 1 institution in 1 country.

Ze-Mou YuDepartment of Neurology, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Xiao-Tao DengDepartment of Radiology, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Ruo-Mei QiThe MOH Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Lu-Yan XiaoDepartment of Laboratory, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Chong-Qing YangDepartment of Pathology, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Tao GongDepartment of Neurology, Beijing Hospital, National Center of Gerontology, Beijing 100730, China.
Beijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic stress contributes to increased risks of atherosclerotic diseases including heart disease, stroke, and transient ischemic attack. However, its underline mechanisms are poorly understood. This study aimed to elucidate the mechanism via which chronic stress exerts its effect on atherosclerosis (AS).

methodsFifty male New Zealand white rabbits were used. Aortic balloon-injury model was applied. Both social stress and physical stress methods were adopted to establish chronic stress models. The lumen stenotic degree, intimal and medial areas, maximum fibrous cap thickness, and plaque contents were measured with histological sections. Proteomic methods were applied to detect protein changes in abdominal aortas to identify the specialized mediators. Real-time reverse transcription-polymerase chain reaction was used for further verification and investigation.

resultsThe stress rabbits exhibited lower body weight, worse fur state, more inactivity behavior, and higher serum cortisol level. Chronic stress was significantly associated with the decreased medial area and increased plaque instability, which was manifested by thinner fibrous caps, larger lipid cores, more macrophages, and new vessels but fewer smooth muscle cells and elastic fibers. After chronic stress, the apoptosis-related genes UBE2K, BAX, FAS, Caspase 3, Caspase 9, and P53 were upregulated, and BCL-2/BAX was down-regulated; the angiogenesis-related genes ANG and VEGF-A were also highly expressed in atherosclerotic arteries.

conclusionsRabbit models of chronic stress were successfully established by applying both social stress and physical stress for 8 weeks. Chronic stress can reduce AS tunica media and accelerate plaque instability by promoting apoptosis and neovascularization.

Indexed as

Stress, PhysiologicalAnimalsApoptosisAtherosclerosisChronic DiseaseDisease Models, AnimalMalePlaque, AtheroscleroticRabbitsStress, PsychologicalTunica Media

Identifiers

PMID29336364
PMCPMC5776846
OpenAlexW2782625396

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.