Evidence map›Paper›PMID 21888911›Full record

ReviewJournal of molecular and cellular cardiology2012

Different subcellular populations of L-type Ca2+ channels exhibit unique regulation and functional roles in cardiomyocytes.

Jabe M Best, Timothy J Kamp

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.1field-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

38 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  9. Review
  10. Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022
    Review
  11. Review
  12. Review
  13. Reconstitution of β-adrenergic regulation of CaProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Studying signal compartmentation in adult cardiomyocytes.Biochemical Society transactions · 2020
    Review
  17. Article
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  19. Review
  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

2 authors at 1 institution in 1 country.

Jabe M BestCellular and Molecular Arrhythmia Research Program, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA.
Timothy J Kamp
University of Wisconsin–Madison · US

Funding

INTEGRATED TRAINING FOR PHYSICIAN-SCIENTISTST32GM008692 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI BURKARD, MARK E · 1998 to 2020
$10.3M
Caveolae and L-type Calcium Channels in CardiomyocytesR01HL078878 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI BALIJEPALLI, RAVI CHANDRA, KAMP, TIMOTHY J. · 2007 to 2016
$3.1M
NHLBI NIH HHS R01 HL078878NIGMS NIH HHS T32 GM008692
6 · The paper itself

Abstract

Influx of Ca(2+) through L-type Ca(2+) channels (LTCCs) contributes to numerous cellular processes in cardiomyocytes including excitation-contraction (EC) coupling, membrane excitability, and transcriptional regulation. Distinct subpopulations of LTCCs have been identified in cardiac myocytes, including those at dyadic junctions and within different plasma membrane microdomains such as lipid rafts and caveolae. These subpopulations of LTCCs exhibit regionally distinct functional properties and regulation, affording precise spatiotemporal modulation of L-type Ca(2+) current (I(Ca,L)). Different subcellular LTCC populations demonstrate variable rates of Ca(2+)-dependent inactivation and sometimes coupled gating of neighboring channels, which can lead to focal, persistent I(Ca,L). In addition, the assembly of spatially defined macromolecular signaling complexes permits compartmentalized regulation of I(Ca,L) by a variety of neurohormonal pathways. For example, β-adrenergic receptor subtypes signal to different LTCC subpopulations, with β(2)-adrenergic activation leading to enhanced I(Ca,L) through caveolar LTCCs and β(1)-adrenergic stimulation modulating LTCCs outside of caveolae. Disruptions in the normal subcellular targeting of LTCCs and associated signaling proteins may contribute to the pathophysiology of a variety of cardiac diseases including heart failure and certain arrhythmias. Further identifying the characteristic functional properties and array of regulatory molecules associated with specific LTCC subpopulations will provide a mechanistic framework to understand how LTCCs contribute to diverse cellular processes in normal and diseased myocardium. This article is part of a Special Issue entitled "Local Signaling in Myocytes".

Indexed as

AnimalsCalcium Channels, L-TypeExcitation Contraction CouplingHeartHeart DiseasesHumansIntracellular SpaceMembrane MicrodomainsMyocytes, CardiacProtein TransportSignal TransductionCalcium Channels, L-Type

Identifiers

PMID21888911
PMCPMC3264751
OpenAlexW2028450256

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.