Evidence map›Paper›PMID 27186946›Full record

ArticleBritish journal of pharmacology2016

Ginkgolide K protects the heart against endoplasmic reticulum stress injury by activating the inositol-requiring enzyme 1α/X box-binding protein-1 pathway.

Shoubao Wang, Zhenzhong Wang, Qiru Fan, Jing Guo, Gina Galli, Guanhua Du, Xin Wang, Wei Xiao

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
13.5field-weighted citation impact, top 1% 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

39 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Molecular Mechanism Underlying Role of the XBP1s in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2022
    Review
  17. Review
  18. Article
  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

8 authors at 3 institutions in 2 countries.

Shoubao WangFaculty of Life Sciences, The University of Manchester, Manchester, UK.
Zhenzhong WangState Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang, China.
Qiru FanState Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang, China.
Jing GuoFaculty of Life Sciences, The University of Manchester, Manchester, UK.
Gina GalliFaculty of Life Sciences, The University of Manchester, Manchester, UK.
Guanhua DuBeijing Key Laboratory of Drug Targets Identification and Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xin WangFaculty of Life Sciences, The University of Manchester, Manchester, UK.
Wei XiaoState Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang, China.
Kanion Pharmaceutical (China) · CNUniversity of Manchester · GBChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

British Heart Foundation PG/09/052/27833British Heart Foundation PG/12/76/29852British Heart Foundation PG/14/70/31039British Heart Foundation PG/14/71/31063
6 · The paper itself

Abstract

background and purposeEndoplasmic reticulum (ER) stress is increasingly recognized as an important causal factor of many diseases. Targeting ER stress has now emerged as a new therapeutic strategy for treating cardiovascular diseases. Here, we investigated the effects and underlying mechanism of ginkgolide K (1,10-dihydroxy-3,14-didehydroginkgolide, GK) on cardiac ER stress. EXPERIMENTAL APPROACH: Cell death, apoptosis and ER stress-related signalling pathways were measured in cultured neonatal rat cardiomyocytes, treated with the ER stress inducers tunicamycin, hydrogen peroxide and thapsigargin. Acute myocardial infarction was established using left coronary artery occlusion in mice, and infarct size was measured by triphenyltetrazolium chloride staining. Echocardiography was used to assess heart function and transmission electron microscopy for evaluating ER expansion. KEY

resultsGinkgolide K (GK) significantly decreased ER stress-induced cell death in both in vitro and in vivo models. In ischaemic injured mice, GK treatment reduced infarct size, rescued heart dysfunction and ameliorated ER dilation. Mechanistic studies revealed that the beneficial effects of GK occurred through enhancement of inositol-requiring enzyme 1α (IRE1α)/X box-binding protein-1 (XBP1) activity, which in turn led to increased ER-associated degradation-mediated clearance of misfolded proteins and autophagy. In addition, GK was also able to partly repress the pro-apoptotic action of regulated IRE1-dependent decay and JNK pathway. CONCLUSIONS AND IMPLICATIONS: In conclusion, GK acts through selective activation of the IRE1α/XBP1 pathway to limit ER stress injury. GK is revealed as a promising therapeutic agent to ameliorate ER stress for treating cardiovascular diseases.

Indexed as

Alternative SplicingAnimalsDose-Response Relationship, DrugEndoplasmic Reticulum StressEndoribonucleasesGinkgolidesHeartLactonesMaleMiceMice, Inbred ICRMyocardiumPhosphorylationProtein Serine-Threonine KinasesRatsRats, Sprague-DawleyEndoribonucleasesErn1 protein, mouseginkgolide KGinkgolidesLactonesProtein Serine-Threonine KinasesRNA, MessengerX-Box Binding Protein 1Xbp1 protein, mouse

Identifiers

PMID27186946
PMCPMC4945765
OpenAlexW2461219810

What OpenQuestion holds

Textmetadata
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.