Evidence map›Paper›PMID 25339116›Full record

ArticleMolecular medicine reports2015

Melatonin alleviates myosin light chain kinase expression and activity via the mitogen-activated protein kinase pathway during atherosclerosis in rabbits.

Xiaowen Cheng, Yufeng Wan, Yuanhong Xu, Qing Zhou, Yuan Wang, Huaqing Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 37% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Evidence for the Benefits of Melatonin in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2022
    Review
  10. Article
  11. Is Melatonin the Cornucopia of the 21st Century?Antioxidants (Basel, Switzerland) · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. 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

6 authors at 3 institutions in 1 country.

Xiaowen ChengLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Yufeng WanDepartment of Otolaryngology, The Affiliated Chaohu Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Yuanhong XuDepartment of Clinical Laboratory, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Qing ZhouLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Yuan WangLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Huaqing ZhuLaboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei, Anhui 230032, P.R. China.
Anhui Medical University · CNChaohu Hospital of Anhui Medical University · CNFirst Affiliated Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin (MLT) is an endogenous indole compound with numerous biological activities that has been associated with atherosclerosis (AS). In the present study, rabbits were used as an AS model in order to investigate whether MLT affects endothelial cell permeability, myosin light chain kinase (MLCK) activity and MLCK expression via the mitogen-activated protein kinase (MAPK) pathway. Expression and activity of MLCK were measured using western blot analysis, quantitative polymerase chain reaction, immunohistochemistry and γ-32P-adenosine triphosphate incorporation. Endothelial permeability was detected using rhodamine phalloidin fluorescence staining. The phosphorylation of extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 in endothelial cells were also analyzed using western blot analysis. Atheromatous plaques were formed in rabbits with a high cholesterol diet; however, following treatment with MLT, the number and areas of atheromatous plaques were significantly reduced. In addition, MLT treatment reversed the increase of MLCK activity and expression that occurred in rabbits with high cholesterol intake. Furthermore, levels of phosphorylated ERK, JNK and p38 decreased following MLT treatment. In conclusion, the results of the present study indicated that AS may be associated with increased MLCK expression and activity, which was reduced following treatment with MLT. The mechanism of action of MLT was thought to proceed via modulating MAPK pathway signal transduction; however, further studies are required in order to fully elucidate the exact regulatory mechanisms involved.

Indexed as

MAP Kinase Signaling SystemAnimalsAortaAtherosclerosisCapillary PermeabilityDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesGene ExpressionJNK Mitogen-Activated Protein KinasesMaleMelatoninMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphorylationPlaque, AtheroscleroticRabbitsExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesMelatoninMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesRNA, Messenger

Identifiers

PMID25339116
PMCPMC4237093
OpenAlexW2133195930

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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.