Evidence map›Paper›PMID 25961164›Full record

ArticleMolecules (Basel, Switzerland)2015

RETRACTED: Celastrol Protects against Antimycin A-Induced Insulin Resistance in Human Skeletal Muscle Cells.

Mohamad Hafizi Abu Bakar, Kian-Kai Cheng, Mohamad Roji Sarmidi, Harisun Yaakob, Hasniza Zaman Huri

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Molecules (Basel, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
7.8field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Journal of traditional and complementary medicine · 2024
    Article
  6. Article
  7. Frontiers in pharmacology · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Evidence-based complementary and alternative medicine : eCAM · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Mohamad Hafizi Abu BakarDepartment of Bioprocess Engineering, Faculty of Chemical Engineering, Universiti Teknologi Malaysia, 81310 Johor Bahru, Johor, Malaysia. mhafizi55@live.utm.my.
Kian-Kai ChengDepartment of Bioprocess Engineering, Faculty of Chemical Engineering, Universiti Teknologi Malaysia, 81310 Johor Bahru, Johor, Malaysia. chengkiankai@cheme.utm.my.
Mohamad Roji SarmidiInnovation Centre in Agritechnology for Advanced Bioprocessing (ICA), Universiti Teknologi Malaysia, 81310 Skudai, Johor, Malaysia. mroji@ibd.utm.my.
Harisun YaakobInstitute of Bioproduct Development, Universiti Teknologi Malaysia, 81310 Johor Bahru, Johor, Malaysia. harisun@ibd.utm.my.
Hasniza Zaman HuriDepartment of Pharmacy, Faculty of Medicine, University of Malaya, 50603 Kuala Lumpur, Malaysia. hasnizazh@ummc.edu.my.
University of Technology Malaysia · MYUniversity of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction and inflammation are widely accepted as key hallmarks of obesity-induced skeletal muscle insulin resistance. The aim of the present study was to evaluate the functional roles of an anti-inflammatory compound, celastrol, in mitochondrial dysfunction and insulin resistance induced by antimycin A (AMA) in human skeletal muscle cells. We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. Furthermore, celastrol prevented increased levels of cellular oxidative damage where the production of several pro-inflammatory cytokines in cultures cells was greatly reduced. Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-κB and PKC θ activation in human skeletal muscle treated with AMA. The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. Taken together, these results suggest that celastrol may be advocated for use as a potential therapeutic molecule to protect against mitochondrial dysfunction-induced insulin resistance in human skeletal muscle cells.

Indexed as

Antimycin ACell LineGlucoseGlucose Transporter Type 4HumansInflammationInsulinInsulin ResistanceMitochondriaMuscle CellsMuscle, SkeletalNF-kappa BPentacyclic TriterpenesPhosphatidylinositol 3-KinasesPhosphorylationProtective AgentsAntimycin AcelastrolGlucoseGlucose Transporter Type 4InsulinNF-kappa BPentacyclic TriterpenesPhosphatidylinositol 3-KinasesProtective AgentsProtein Kinase CProto-Oncogene Proteins c-aktTriterpenes

Identifiers

PMID25961164
PMCPMC6272652
OpenAlexW1502976945

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.