Evidence map›Paper›PMID 27550383›Full record

ArticleScientific reports2016

Inhibition of endoplasmic reticulum stress improves coronary artery function in the spontaneously hypertensive rats.

Soo-Kyoung Choi, Mihwa Lim, Seon-Hee Byeon, Young-Ho Lee

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Emerging role of IRE1α in vascular diseases.Journal of cell communication and signaling · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Mechanisms of Oxidative Stress in Metabolic Syndrome.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Oxidative Stress and Hypertension.Circulation research · 2021
    Review
  16. Article
  17. Article
  18. Mechanical Regulation of Protein Translation in the Cardiovascular System.Frontiers in cell and developmental biology · 2020
    Review
  19. Article
  20. 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

4 authors.

Soo-Kyoung ChoiDepartment of Physiology, College of Medicine, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University, Seoul, Korea.
Mihwa LimDepartment of Physiology, College of Medicine, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University, Seoul, Korea.
Seon-Hee ByeonDepartment of Physiology, College of Medicine, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University, Seoul, Korea.
Young-Ho LeeDepartment of Physiology, College of Medicine, Brain Korea 21 Plus Project for Medical Sciences, Yonsei University, Seoul, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress has been shown to play a critical role in the pathogenesis of cardiovascular complications. However, the role and mechanisms of ER stress in hypertension remain unclear. Thus, we hypothesized that enhanced ER stress contributes to the maintenance of hypertension in spontaneously hypertensive rats (SHRs). Sixteen-week old male SHRs and Wistar Kyoto Rats (WKYs) were used in this study. The SHRs were treated with ER stress inhibitor (Tauroursodeoxycholic acid; TUDCA, 100 mg/kg/day) for two weeks. There was a decrease in systolic blood pressure in SHR treated with TUDCA. The pressure-induced myogenic tone was significantly increased, whereas endothelium-dependent relaxation was significantly attenuated in SHR compared with WHY. Interestingly, treatment of ER stress inhibitor normalized myogenic responses and endothelium-dependent relaxation in SHR. These data were associated with an increase in expression or phosphorylation of ER stress markers (Bip, ATF6, CHOP, IRE1, XBP1, PERK, and eIF2α) in SHRs, which were reduced by TUDCA treatment. Furthermore, phosphorylation of MLC20 was increased in SHRs, which was reduced by the treatment of TUDCA. Therefore, our results suggest that ER stress could be a potential target for hypertension.

Indexed as

AnimalsBiomarkersCoronary VesselsDisease Models, AnimalDrug Administration ScheduleEndoplasmic Reticulum StressGene Expression RegulationHypertensionMalePhosphorylationRatsRats, Inbred SHRRats, Inbred WKYTaurochenodeoxycholic AcidBiomarkersTaurochenodeoxycholic Acidursodoxicoltaurine

Identifiers

PMID27550383
PMCPMC4994042

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.