Evidence map›Paper›PMID 20105174›Full record

ArticleBritish journal of pharmacology2010

Tetrandrine blocks cardiac hypertrophy by disrupting reactive oxygen species-dependent ERK1/2 signalling.

Di-Fei Shen, Qi-Zhu Tang, Ling Yan, Yan Zhang, Li-Hua Zhu, Lang Wang, Chen Liu, Zhou-Yan Bian, Hongliang Li

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.5field-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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  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

9 authors at 3 institutions in 1 country.

Di-Fei ShenDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.
Qi-Zhu Tang
Ling Yan
Yan Zhang
Li-Hua Zhu
Lang Wang
Chen Liu
Zhou-Yan Bian
Hongliang Li
Renmin Hospital of Wuhan University · CNWuhan University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeTetrandrine, a well-known naturally occurring calcium antagonist with anti-inflammatory, antioxidant and anti-fibrogenetic activities, has long been used clinically for treatment of cardiovascular diseases such as hypertension and arrhythmia. However, little is known about the effect of tetrandrine on cardiac hypertrophy. The aims of the present study were to determine whether tetrandrine could attenuate cardiac hypertrophy and to clarify the underlying molecular mechanisms. EXPERIMENTAL APPROACH: Tetrandrine (50 mg x kg(-1) x day(-1)) was administered by oral gavage three times a day for one week and then the mice were subjected to either chronic pressure overload generated by aortic banding (AB) or sham surgery (control group). Cardiac function was determined by echocardiography. KEY

resultsTetrandrine attenuated the cardiac hypertrophy induced by AB, as assessed by heart weight/body weight and lung weight/body weight ratios, cardiac dilatation and the expression of genes of hypertrophic markers. Tetrandrine also inhibited fibrosis and attenuated the inflammatory response. The cardioprotective effects of tetrandrine were mediated by blocking the increased production of reactive oxygen species and the activation of ERK1/2-dependent nuclear factor-kappaB and nuclear factor of activated T cells that occur in response to hypertrophic stimuli. CONCLUSIONS AND IMPLICATIONS: Taken together, our results suggest that tetrandrine can improve cardiac function and prevent the development of cardiac hypertrophy by suppressing the reactive oxygen species-dependent ERK1/2 signalling pathway.

Indexed as

Administration, OralAnimalsAnimals, NewbornAnti-Inflammatory AgentsAntioxidantsApoptosisBenzylisoquinolinesCardiomegalyCardiotonic AgentsCells, CulturedDisease Models, AnimalEnzyme ActivationFibrosisHeart FailureMiceMitogen-Activated Protein Kinase 1Anti-Inflammatory AgentsAntioxidantsBenzylisoquinolinesCardiotonic AgentsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NFATC Transcription FactorsNF-kappa BReactive Oxygen Speciestetrandrine

Identifiers

PMID20105174
PMCPMC2829222
OpenAlexW2128837905

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.