Evidence map›Paper›PMID 20951705›Full record

ArticleJournal of molecular and cellular cardiology2011

Expression and roles of Cav1.3 (α1D) L-type Ca²+ channel in atrioventricular node automaticity.

Qian Zhang, Valeriy Timofeyev, Hong Qiu, Ling Lu, Ning Li, Anil Singapuri, Cyril L Torado, Hee-Sup Shin, Nipavan Chiamvimonvat

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Impact of CaInternational journal of molecular sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pharmacologic Approach to Sinoatrial Node Dysfunction.Annual review of pharmacology and toxicology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Transmural gradients in ion channel and auxiliary subunit expression.Progress in biophysics and molecular biology · 2016
    Review
  15. Interactions of Short-Term and Chronic Treadmill Training With Aging of the Left Ventricle of the Heart.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016
    Article
  16. Article
  17. Review
  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 2 institutions in 3 countries.

Qian ZhangDivision of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA.
Valeriy Timofeyev
Hong Qiu
Ling Lu
Ning Li
Anil Singapuri
Cyril L Torado
Hee-Sup Shin
Nipavan Chiamvimonvat
University of California, Davis · USKorea Institute of Science and Technology · KR

Funding

Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Functions of calcium-activated ion channels in the heartR01HL075274 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2004 to 2007
$1.5M
NHLBI NIH HHS HL085844NHLBI NIH HHS R01 HL075274NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844
6 · The paper itself

Abstract

Atrioventricular node (AV node) is the hub where electrical input from the atria is propagated and conveyed to the ventricles. Despite its strategic position and role in governing impulse conduction between atria and ventricles, there is paucity of data regarding the contribution of specific ion channels to the function of the AV node. Here, we examined the roles of Ca(v)1.3 L-type Ca(2+) channel in AV node by taking advantage of a mouse model with null mutation of Ca(v)1.3 (Ca(v)1.3(-/-)). Ca(v)1.3 null mutant mice show evidence of AV node dysfunction with AV block, suggesting the tissue-specific function of the Ca(v)1.3 channel. In keeping with this assertion, we demonstrate that Ca(v)1.3 isoform is highly expressed in the isolated AV node cells. Furthermore, AV node isolated from Ca(v)1.3 null mutant mice show a significant decrease in the firing frequency of spontaneous action potentials suggesting that Ca(v)1.3 L-type Ca(2+) channel plays significant roles in the automaticity of the AV node. Because of the distinct voltage-dependence of Ca(v)1.2 and Ca(v)1.3 Ca(2+) channels, Ca(v)1.2 alone does not suffice to maintain normal AV node function. Ca(v)1.3 currents activate at more hyperpolarizing voltage compared to Ca(v)1.2 currents. Consequently, Ca(v)1.2 Ca(2+) channel cannot functionally substitute for Ca(v)1.3 isoform in the AV node of Ca(v)1.3 null mutant mice. Thus, our study demonstrates that the distinct biophysical properties of Ca(v)1.3 Ca(2+) channel play critical roles in the firing frequency of AV node tissues.

Indexed as

Action PotentialsAnimalsAtrioventricular NodeCalcium Channels, L-TypeImmunohistochemistryMiceMice, Mutant StrainsMicroscopy, ConfocalModels, TheoreticalPatch-Clamp TechniquesCacna1d protein, mouseCalcium Channels, L-Type

Identifiers

PMID20951705
PMCPMC3680510
OpenAlexW1997617562

What OpenQuestion holds

Textmetadata
LicenceTDM
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.