Evidence map›Paper›PMID 18940894›Full record

ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009

Physiology and pathophysiology of canonical transient receptor potential channels.

Joel Abramowitz, Lutz Birnbaumer

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 170 papers.

0numbers the graph read from it
0cells of the map it votes in
170citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

170 citing papers in PubMed, 330 citations in OpenAlex.

  1. TRPC6-Mediated CaCells · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. CaBiomedicines · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. TRPC3 Is Downregulated in Primary Hyperparathyroidism.International journal of molecular sciences · 2024
    Article
  10. Transient Receptor Potential Channels in the Healthy and Diseased Blood-Brain Barrier.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022
    Review
  15. Article
  16. Article
  17. Review
  18. The Wnt Signaling Pathway in Diabetic Nephropathy.Frontiers in cell and developmental biology · 2021
    Review
  19. Article
  20. Article

110 more citing papers are in PubMed but not listed here.

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.

Joel AbramowitzTransmembrane Signaling Group, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. abramow1@niehs.nih.gov
Lutz Birnbaumer
National Institutes of Health · US

Funding

Transmembrane Signaling Mechanisms Involving TRP ChannelsZIGES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2009 to 2010
$2.1M
Transmembrane Signaling Mechanisms Involving TRP ChannelsZ01ES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$2.1M
Intramural NIH HHS Z01 ES101684
6 · The paper itself

Abstract

The existence of a mammalian family of TRPC ion channels, direct homologues of TRP, the visual transduction channel of flies, was discovered during 1995-1996 as a consequence of research into the mechanism by which the stimulation of the receptor-Gq-phospholipase Cbeta signaling pathway leads to sustained increases in intracellular calcium. Mammalian TRPs, TRPCs, turned out to be nonselective, calcium-permeable cation channels, which cause both a collapse of the cell's membrane potential and entry of calcium. The family comprises 7 members and is widely expressed. Many cells and tissues express between 3 and 4 of the 7 TRPCs. Despite their recent discovery, a wealth of information has accumulated, showing that TRPCs have widespread roles in almost all cells studied, including cells from excitable and nonexcitable tissues, such as the nervous and cardiovascular systems, the kidney and the liver, and cells from endothelia, epithelia, and the bone marrow compartment. Disruption of TRPC function is at the root of some familial diseases. More often, TRPCs are contributing risk factors in complex diseases. The present article reviews what has been uncovered about physiological roles of mammalian TRPC channels since the time of their discovery. This analysis reveals TRPCs as major and unsuspected gates of Ca(2+) entry that contribute, depending on context, to activation of transcription factors, apoptosis, vascular contractility, platelet activation, and cardiac hypertrophy, as well as to normal and abnormal cell proliferation. TRPCs emerge as targets for a thus far nonexistent field of pharmacological intervention that may ameliorate complex diseases.

Indexed as

AnimalsCell Physiological PhenomenaDiseaseHumansProtein IsoformsSignal TransductionTransient Receptor Potential ChannelsProtein IsoformsTransient Receptor Potential Channels

Identifiers

PMID18940894
PMCPMC2630793
OpenAlexW2089441515

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.