Evidence map›Paper›PMID 23935402›Full record

ArticleInternational journal of medical sciences2013

Arrhythmogenesis toxicity of aconitine is related to intracellular ca(2+) signals.

Yu-hong Zhou, Xian-mei Piao, Xue Liu, Hai-hai Liang, Lei-min Wang, Xue-hui Xiong, Lu Wang, Yan-jie Lu, Hong-li Shan

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Frontiers in pharmacology · 2026
    Review
  3. Integrated toxicology ofFrontiers in pharmacology · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Processed lateral root ofFrontiers in pharmacology · 2022
    Review
  11. Article
  12. Inhibition of the IActa pharmacologica Sinica · 2021
    Article
  13. Article
  14. Aconitine Induces TRPV2-Mediated CaEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  15. Review
  16. Article
  17. Potential Molecular Mechanisms and Drugs for Aconitine-Induced Cardiotoxicity in Zebrafish through RNA Sequencing and Bioinformatics Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  18. Review
  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 1 institution in 1 country.

Yu-hong ZhouDepartment of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
Xian-mei Piao
Xue Liu
Hai-hai Liang
Lei-min Wang
Xue-hui Xiong
Lu Wang
Yan-jie Lu
Hong-li Shan
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aconitine is a well-known arrhythmogenic toxin and induces triggered activities through cardiac voltage-gated Na(+) channels. However, the effects of aconitine on intracellular Ca(2+) signals were previously unknown. We investigated the effects of aconitine on intracellular Ca(2+) signals in rat ventricular myocytes and explored the possible mechanism of arrhythmogenic toxicity induced by aconitine. Ca(2+) signals were evaluated by measuring L-type Ca(2+) currents, caffeine-induced Ca(2+) release and the expression of NCX and SERCA2a. Action potential and triggered activities were recorded by whole-cell patch-clamp techniques. In rat ventricular myocytes, the action potential duration was significantly prolonged by 1 µM aconitine. At higher concentrations (5 µM and 10 µM), aconitine induced triggered activities and delayed after-depolarizations (6 of 8 cases), which were inhibited by verapamil. Aconitine (1 µM) significantly increased the ICa-L density from 12.77 ± 3.12 pA/pF to 18.98 ± 3.89 pA/pF (n=10, p<0.01). The activation curve was shifted towards more negative potential, while the inactivation curve was shifted towards more positive potential by 1 μM aconitine. The level of Ca(2+) release induced by 10 mM caffeine was markedly increased. Aconitine (1 µM) increased the expression of NCX, while SERCA2a expression was reduced. In conclusion, aconitine increased the cytosolic [Ca(2+)]i by accelerating ICa-L and changing the expression of NCX and SERCA2a. Then, the elevation of cytosolic [Ca(2+)]i induced triggered activities and delayed after-depolarizations. Arrhythmogenesis toxicity of aconitine is related to intracellular Ca(2+) signals.

Indexed as

AconitineAnimalsArrhythmias, CardiacBlotting, WesternCaffeineCalciumCells, CulturedMaleMyocytes, CardiacPatch-Clamp TechniquesRatsRats, WistarSarcoplasmic Reticulum Calcium-Transporting ATPasesAconitineCaffeineCalciumSarcoplasmic Reticulum Calcium-Transporting ATPasesAconitinearrhythmiascaffeine-induced Ca2+ releaseL-type Ca2+ currentNCXSERCA2a

Identifiers

PMID23935402
PMCPMC3739024
OpenAlexW2120607848

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.