Evidence map›Paper›PMID 21814047›Full record

ArticleChannels (Austin, Tex.)

Mice lacking functional TRPV1 are protected from pressure overload cardiac hypertrophy.

Cadie L Buckley, Alexander J Stokes

Open access · goldAbstract read
In one paragraph

Article in Channels (Austin, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  11. Article
  12. TRPV2 channel as a possible drug target for the treatment of heart failure.Laboratory investigation; a journal of technical methods and pathology · 2020
    Review
  13. Article
  14. CaJournal of cardiovascular development and disease · 2019
    Review
  15. Article
  16. Review
  17. Review
  18. Cannabinoids, the Heart of the Matter.Journal of the American Heart Association · 2018
    Review
  19. The endocannabinoid system in cardiovascular function: novel insights and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2018
    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 2 institutions in 1 country.

Cadie L BuckleyCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, USA.
Alexander J Stokes
University of Hawaiʻi at Mānoa · USUniversity of Hawaii System · US

Funding

USING EEG COMPLEXITY AND HIGH PERFORMANCE COMPUTING TO PROFILE SLEEPP20RR016467 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI HOLMES, ERIC · 2001 to 2011
$24.5M
UHI COBRE: SOLID STATE NMR STUDIES OF MINERALIZED ELASTINP20RR016453 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI SHOHET, RALPH V. · 2001 to 2011
$21.2M
RESEARCH DESIGN AND BIOSTATISTICS COREU54MD007584 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI MOKUAU, NOREEN, SHIRAMIZU, BRUCE T · 2012 to 2018
$21.1M
RESEARCH ETHICSU54RR026136 · NCRR · UNIVERSITY OF HAWAII AT MANOA · PI SETO, TODD B · 2010 to 2011
$8.5M
U of HI Research Scientist Award in Molecular CardiologyUH1HL073449 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI SHOHET, RALPH V. · 2004 to 2011
$4.1M
Chaminade University BRIC ProjectP20MD006084 · NIMHD · CHAMINADE UNIVERSITY OF HONOLULU · PI PLOEGER, BERNARD · 2010 to 2014
$4.0M
NCRR NIH HHS 5P20RR016453NCRR NIH HHS P20 RR016453NCRR NIH HHS P20 RR016467NCRR NIH HHS P20RR016467NCRR NIH HHS U54 RR026136NCRR NIH HHS U54RR026136NHLBI NIH HHS 5UH1HL073449NHLBI NIH HHS UH1 HL073449NIMHD NIH HHS P20 MD006084NIMHD NIH HHS P20MD06084NIMHD NIH HHS U54 MD007584
6 · The paper itself

Abstract

TRPV1 (transient receptor potential cation channel, subfamily V, member 1) is best studied in peripheral sensory neurons as a pain receptor; however TRPV1 is expressed in numerous tissues and cell types including those of the cardiovascular system. TRPV1 expression is upregulated in the hypertrophic heart, and the channel is positioned to receive stimulatory signals in the hypertrophic heart. We hypothesized that TRPV1 has a role in regulating cardiac hypertrophy. Using transverse aortic constriction to model pressure overload cardiac hypertrophy we show that mice lacking functional TRPV1, compared to wild type, have improved heart function, and reduced hypertrophic, fibrotic and apoptotic markers. This suggests that TRPV1 plays a role in the progression of cardiac hypertrophy, and presents a possible therapeutic target for the treatment of cardiac hypertrophy and heart failure.

Indexed as

AnimalsCardiomegalyDisease Models, AnimalHeart FailureMiceMice, KnockoutMuscle ProteinsMyocardiumTRPV Cation ChannelsUp-RegulationMuscle ProteinsTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID21814047
PMCPMC3225734
OpenAlexW2026191400

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.