Evidence map›Paper›PMID 24161125›Full record

ReviewAntioxidants & redox signaling2014

Redox regulation of neuronal voltage-gated calcium channels.

Slobodan M Todorovic, Vesna Jevtovic-Todorovic

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.0field-weighted citation impact, top 25% 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, 38 citations in OpenAlex.

  1. Article
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  14. Reactive Oxygen Species Modulate Activity-Dependent AMPA Receptor Transport inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  15. Neuronal Cav3 channelopathies: recent progress and perspectives.Pflugers Archiv : European journal of physiology · 2020
    Review
  16. Article
  17. A NeurotoxicFrontiers in molecular neuroscience · 2020
    Review
  18. Review
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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.

Slobodan M Todorovic1 Department of Anesthesiology, University of Virginia School of Medicine , Charlottesville, Virginia.
Vesna Jevtovic-Todorovic
University of Virginia · US

Funding

The role of trace metals and T-channels in painR21DA034448 · NIDA · UNIVERSITY OF VIRGINIA · PI TODOROVIC, SLOBODAN M. · 2013 to 2014
$395k
NIDA NIH HHS R21 DA034448
6 · The paper itself

Abstract

significanceVoltage-gated calcium channels are ubiquitously expressed in neurons and are key regulators of cellular excitability and synaptic transmitter release. There is accumulating evidence that multiple subtypes of voltage-gated calcium channels may be regulated by oxidation and reduction. However, the redox mechanisms involved in the regulation of channel function are not well understood. RECENT ADVANCES: Several studies have established that both T-type and high-voltage-activated subtypes of voltage-gated calcium channel can be redox-regulated. This article reviews different mechanisms that can be involved in redox regulation of calcium channel function and their implication in neuronal function, particularly in pain pathways and thalamic oscillation. CRITICAL ISSUES: A current critical issue in the field is to decipher precise mechanisms of calcium channel modulation via redox reactions. In this review we discuss covalent post-translational modification via oxidation of cysteine molecules and chelation of trace metals, and reactions involving nitric oxide-related molecules and free radicals. Improved understanding of the roles of redox-based reactions in regulation of voltage-gated calcium channels may lead to improved understanding of novel redox mechanisms in physiological and pathological processes. FUTURE DIRECTIONS: Identification of redox mechanisms and sites on voltage-gated calcium channel may allow development of novel and specific ion channel therapies for unmet medical needs. Thus, it may be possible to regulate the redox state of these channels in treatment of pathological process such as epilepsy and neuropathic pain.

Indexed as

Oxidation-ReductionAnimalsAntioxidantsCalciumCalcium ChannelsCalcium Channels, T-TypeCatalysisCysteineHumansMetalsNeuronsNitric OxideProtein IsoformsThioctic AcidAntioxidantsCalciumCalcium ChannelsCalcium Channels, T-TypeCysteineMetalsNitric OxideProtein IsoformsThioctic Acid

Identifiers

PMID24161125
PMCPMC4116091
OpenAlexW1537441151

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.