Evidence map›Paper›PMID 22443172›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)2012

Dynamic Ca(2+) signal modalities in the vascular endothelium.

Mark S Taylor, Michael Francis, Xun Qian, Viktoriya Solodushko

Abstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Guidelines for evaluating endothelial function in vascular tissue.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  2. Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023
    Review
  3. Article
  4. Cenerimod, a novel selective S1PPharmacology research & perspectives · 2017
    Article
  5. Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016
    Review
  6. Article
  7. Automated analysis of dynamic Ca2+ signals in image sequences.Journal of visualized experiments : JoVE · 2014
    Article
  8. 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

4 authors.

Mark S TaylorDepartment of Physiology, University of South Alabama College of Medicine, Mobile, Alabama 36688, USA. mtaylor@usouthal.edu
Michael Francis
Xun Qian
Viktoriya Solodushko

Funding

Coronary Artery Regulation by Small Conduction Ca2+-activated K+ ChannelsR01HL085887 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI TAYLOR, MARK STEPHEN · 2007 to 2011
$1.3M
Request for a Spectral Confocal MicroscopeS10RR027535 · NCRR · UNIVERSITY OF SOUTH ALABAMA · PI RICH, THOMAS C · 2010 to 2010
$397k
NCRR NIH HHS S10 RR027535NCRR NIH HHS S10RR027535NHLBI NIH HHS HL085887NHLBI NIH HHS R01 HL085887
6 · The paper itself

Abstract

The endothelium is vital to normal vasoregulation. Although acute vasodilation associated with broad endothelial Ca(2+) elevation is well known, the control and targeting of Ca(2+) -dependent signals in the endothelium are poorly understood. Recent studies have revealed localized IP(3) -motivated Ca(2+) events occurring basally along the intima that may provide the fundamental basis for various endothelial influences. Here, we provide an overview of dynamic endothelial Ca(2+) signals and discuss the potential role of these signals in constant endothelial control of arterial tone and the titration of functional responses in vivo. In particular, we focus on the functional architecture contributing to the properties and ultimate impact of these signals, and explore new avenues in evaluating their prevalence and specific modalities in intact tissue. Finally, we discuss spatial and temporal effector recruitment through modification of these inherent signals. It is suggested that endothelial Ca(2+) signaling is a continuum in which the specific framework of store-release components and cellular targets along the endothelium allows for differential modes of Ca(2+) signal expansion and distinctive profiles of effector recruitment. The precise composition and distribution of these inherent components may underlie dynamic endothelial control and specialized functions of different vascular beds.

Indexed as

AnimalsArteriesCalciumCalcium SignalingEndothelium, VascularHemodynamicsHumansInositol 1,4,5-TrisphosphateMuscle TonusCalciumInositol 1,4,5-Trisphosphate

Identifiers

PMID22443172
PMCPMC3393781

What OpenQuestion holds

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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.