Evidence map›Paper›PMID 24886224›Full record

ArticleCardiovascular diabetology2014

Inhibition of calpain reduces oxidative stress and attenuates endothelial dysfunction in diabetes.

Bainian Chen, Qing Zhao, Rui Ni, Futian Tang, Limei Shan, Inga Cepinskas, Gediminas Cepinskas, Wang Wang, Peter W Schiller, Tianqing Peng

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2014. 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
3.3field-weighted citation impact, top 8% 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, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Recent Advances inGels (Basel, Switzerland) · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

10 authors at 6 institutions in 3 countries.

Bainian Chen
Qing Zhao
Rui Ni
Futian Tang
Limei Shan
Inga Cepinskas
Gediminas Cepinskas
Wang Wang
Peter W Schiller
Tianqing PengInstitute for Cardiovascular Science of Soochow University, Suzhou, Jiangsu Province 215123, China. tqpeng@suda.edu.cn.
London Health Sciences Centre · CALawson Health Research Institute · CAWestern University · CAMontreal Clinical Research Institute · CAShanghai Jiao Tong University · CNUniversity of Washington · US

Funding

DEVELOPMENT OF RECEPTOR-SPECIFIC OPIOID PEPTIDE ANALOGSR01DA004443 · NIDA · CLINICAL RESEARCH INSTITUTE OF MONTREAL · PI SCHILLER, PETER W · 1987 to 2016
$2.0M
DEVELOPMENT OF RECEPTOR SPECIFIC OPIOID PEPTIDE ANALOGSR37DA004443 · NIDA · CLINICAL RESEARCH INSTITUTE OF MONTREAL · PI SCHILLER, PETER W · 1997 to 2003
$621k
CIHRNIDA NIH HHS DA-004443NIDA NIH HHS R01 DA004443
6 · The paper itself

Abstract

aimsThe present study was to investigate the role of calpain in reactive oxygen species (ROS) production in endothelial cells and endothelium-dependent vascular dysfunction under experimental conditions of diabetes. METHODS AND

resultsExposure to high glucose activated calpain, induced apoptosis and reduced nitric oxide (NO) production without changing eNOS protein expression, its phosphorylation and dimers formation in primary human umbilical vein endothelial cells (HUVECs). These effects of high glucose correlated with intracellular ROS production and mitochondrial superoxide generation. Selectively scavenging mitochondrial superoxide increased NO production in high glucose-stimulated HUVECs. Inhibition of calpain using over-expression of calpastatin or pharmacological calpain inhibitor prevented high glucose-induced ROS production, mitochondrial superoxide generation and apoptosis, which were concurrent with an elevation of NO production in HUVECs. In mouse models of streptozotocin-induced type-1 diabetes and OVE26 type-1 diabetic mice, calpain activation correlated with an increase in ROS production and peroxynitrite formation in aortas. Transgenic over-expression of calpastatin reduced ROS production and peroxynitrite formation in diabetic mice. In parallel, diabetes-induced reduction of endothelium-dependent relaxation in aortic ring was reversed by over-expression of calpastatin in mouse models of diabetes. However, the protective effect of calpastatin on endothelium-dependent relaxation was abrogated by eNOS deletion in diabetic mice.

conclusionsThis study suggests that calpain may play a role in vascular endothelial cell ROS production and endothelium-dependent dysfunction in diabetes. Thus, calpain may be an important therapeutic target to overcome diabetes-induced vascular dysfunction.

Indexed as

AnimalsCalpainDiabetes MellitusEndothelium, VascularGlycoproteinsHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred C57BLMice, TransgenicOrgan Culture TechniquesOxidative StressReactive Oxygen SpeciesCalpaincalpain inhibitorsGlycoproteinsReactive Oxygen Species

Identifiers

PMID24886224
PMCPMC4045988
OpenAlexW2158237738

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.