Evidence map›Paper›PMID 20201820›Full record

ReviewCNS & neurological disorders drug targets2010

TRPC channels and their implication in neurological diseases.

Senthil Selvaraj, Yuyang Sun, Brij B Singh

Open access · greenAbstract readReview
In one paragraph

Review in CNS & neurological disorders drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. TRPC4/5 inhibitors: Phase I results and proof of concept studies.European archives of psychiatry and clinical neuroscience · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. How TRPC Channels Modulate Hippocampal Function.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Memory and Learning Deficits Are Associated With CaFrontiers in aging neuroscience · 2020
    Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Structure of the mouse TRPC4 ion channel.Nature communications · 2018
    Article
  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

3 authors at 1 institution in 1 country.

Senthil SelvarajDepartment of Biochemistry and Molecular Biology, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58201, USA.
Yuyang Sun
Brij B Singh
University of North Dakota · US

Funding

TRPC1, CALCIUM AND PARKINSON'S DISEASEP20RR017699 · NCRR · UNIVERSITY OF NORTH DAKOTA · PI GROVE, BRYON D · 2002 to 2011
$19.7M
TRPC1, Calcium, and Saliva SecretionR01DE017102 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Brij B Singh · 2006 to 2026
$7.5M
NCRR NIH HHS 5P20RR017699NCRR NIH HHS P20 RR017699NIDCR NIH HHS DE017102NIDCR NIH HHS R01 DE017102
6 · The paper itself

Abstract

Calcium is an essential intracellular messenger and serves critical cellular functions in both excitable and non-excitable cells. Most of the physiological functions in these cells are uniquely regulated by changes in cytosolic Ca2+ levels ([Ca2+](i)), which are achieved via various mechanisms. One of these mechanism(s) is activated by the release of Ca2+ from the endoplasmic reticulum (ER), followed by Ca2+ influx across the plasma membrane (PM). Activation of PM Ca2+ channel is essential for not only refilling of the ER Ca2+ stores, but is also critical for maintaining [Ca2+](i) that regulates biological functions, such as neurosecretion, sensation, long term potentiation, synaptic plasticity, gene regulation, as well as cellular growth and differentiation. Alterations in Ca2+ homeostasis have been suggested in the onset/progression of neurological diseases, such as Parkinson's, Alzheimer's, bipolar disorder, and Huntington's. Available data on transient receptor potential conical (TRPC) protein indicate that these proteins initiate Ca2+ entry pathways and are essential in maintaining cytosolic, ER, and mitochondrial Ca2+ levels. A number of biological functions have been assigned to these TRPC proteins. Silencing of TRPC1 and TRPC3 has been shown to inhibit neuronal proliferation and loss of TRPC1 is implicated in neurodegeneration. Thus, TRPC channels not only contribute towards normal physiological processes, but are also implicated in several human pathological conditions. Overall, it is suggested that these channels could be used as potential therapeutic targets for many of these neurological diseases. Thus, in this review we have focused on the functional implication of TRPC channels in neuronal cells along with the elucidation of their role in neurodegeneration.

Indexed as

AnimalsBrainCalciumCalcium SignalingCytosolEndoplasmic ReticulumHumansMitochondriaNeurocognitive DisordersNeurodegenerative DiseasesNeuronsTRPC Cation ChannelsCalciumTRPC Cation Channels

Identifiers

PMID20201820
PMCPMC2846610
OpenAlexW2127897062

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.