Evidence map›Paper›PMID 25041185›Full record

ArticleBritish journal of pharmacology2014

Celastrol protects ischaemic myocardium through a heat shock response with up-regulation of haeme oxygenase-1.

S Der Sarkissian, J-F Cailhier, M Borie, L-M Stevens, L Gaboury, S Mansour, P Hamet, N Noiseux

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Transient Increase in ATInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Prevention and Treatment of Cardiovascular Diseases with Plant Phytochemicals: A Review.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  13. Exploring the Pharmacological Mechanisms ofBioMed research international · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Protective effect of celastrol for burn-induced acute lung injury in rats.International journal of clinical and experimental pathology · 2019
    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

8 authors at 3 institutions in 1 country.

S Der SarkissianCentre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Quebec, Canada; Department of Surgery, Université de Montréal, Montreal, Quebec, Canada.
J-F Cailhier
M Borie
L-M Stevens
L Gaboury
S Mansour
P Hamet
N Noiseux
Centre Hospitalier de l’Université de Montréal · CAInstitute for Research in Immunology and Cancer · CAUniversité de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeCelastrol, a triterpene from plants, has been used in traditional oriental medicine to treat various diseases. Here, we investigated the cardioprotective effects of celastrol against ischaemia. EXPERIMENTAL APPROACH: Protective pathways induced by celastrol were investigated in hypoxic cultures of H9c2 rat cardiomyoblasts and in a rat model of myocardial infarction, assessed with echocardiographic and histological analysis. KEY

resultsIn H9c2 cells, celastrol triggered reactive oxygen species (ROS) formation within minutes, induced nuclear translocation of the transcription factor heat shock factor 1 (HSF1) resulting in a heat shock response (HSR) leading to increased expression of heat shock proteins (HSPs). ROS scavenger N-acetylcysteine reduced expression of HSP70 and HSP32 (haeme oxygenase-1, HO-1). Celastrol improved H9c2 survival under hypoxic stress, and functional analysis revealed HSF1 and HO-1 as key effectors of the HSR, induced by celastrol, in promoting cytoprotection. In the rat ischaemic myocardium, celastrol treatment improved cardiac function and reduced adverse left ventricular remodelling at 14 days. Celastrol triggered expression of cardioprotective HO-1 and inhibited fibrosis and infarct size. In the peri-infarct area, celastrol reduced myofibroblast and macrophage infiltration, while attenuating up-regulation of TGF-β and collagen genes. CONCLUSIONS AND IMPLICATIONS: Celastrol treatment induced an HSR through activation of HSF1 with up-regulation of HO-1 as the key effector, promoting cardiomyocyte survival, reduction of injury and adverse remodelling with preservation of cardiac function. Celastrol may represent a novel potent pharmacological cardioprotective agent mimicking ischaemic conditioning that could have a valuable impact in the treatment of myocardial infarction.

Indexed as

AnimalsCardiotonic AgentsCell LineCell SurvivalDNA-Binding ProteinsFemaleHeat-Shock ResponseHeat Shock Transcription FactorsHeme Oxygenase (Decyclizing)HSP70 Heat-Shock ProteinsHypoxiaMAP Kinase Signaling SystemMyocardial IschemiaMyocardiumOncogene Protein v-aktPentacyclic TriterpenesCardiotonic AgentscelastrolDNA-Binding ProteinsHeat Shock Transcription FactorsHeme Oxygenase (Decyclizing)Hmox1 protein, ratHsf1 protein, ratHSP70 Heat-Shock ProteinsOncogene Protein v-aktPentacyclic TriterpenesPhosphatidylinositol 3-KinasesReactive Oxygen SpeciesTranscription FactorsTriterpenes

Identifiers

PMID25041185
PMCPMC4294039
OpenAlexW1953694301

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.