Evidence map›Paper›PMID 19201994›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Reversal of cardiac myocyte dysfunction as a unique mechanism of rescue by P2X4 receptors in cardiomyopathy.

Jian-Bing Shen, Robin Shutt, Mariela Agosto, Achilles Pappano, Bruce T Liang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Effects of ATP administration on isolated swine hearts: Implications forExperimental biology and medicine (Maywood, N.J.) · 2019
    Article
  3. Article
  4. Review
  5. Cardiac P2X purinergic receptors as a new pathway for increasing Na⁺ entry in cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2014
    Article
  6. Article
  7. Article
  8. The therapeutic effect of 2-cyclohexylthio-AMP in heart failure.Journal of cardiovascular pharmacology · 2013
    Article
  9. Review
  10. Article
  11. 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

5 authors at 1 institution in 1 country.

Jian-Bing ShenPat and Jim Calhoun Cardiovascular Center, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
Robin Shutt
Mariela Agosto
Achilles Pappano
Bruce T Liang
UConn Health · US

Funding

PURINERGIC SIGNALING IN CULTURED HEART CELLSR01HL048225 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI LIANG, BRUCE T · 1993 to 2005
$1.9M
NHLBI NIH HHS R01-HL-48225
6 · The paper itself

Abstract

Binary cardiac transgenic (Tg) overexpression of P2X(4) receptors (P2X(4)R) improved the survival of the cardiomyopathic calsequestrin (CSQ) mice. Here we studied the mechanism of rescue using binary P2X(4)R/CSQ Tg and CSQ Tg mice as models. Cellular and intact heart properties were determined by simultaneous sarcomere shortening (SS) and Ca(2+) transients in vitro and echocardiography in vivo. Similar to a delay in death, binary mice exhibited a slowed heart failure progression with a greater left ventricular (LV) fractional shortening (FS) and thickness and a concomitant lesser degree of LV dilatation in both systole and diastole at 8 or 12 wk. By 16 wk, binary hearts showed similarly depressed FS and thinned out LV and equal enlargement of LV as did 12-wk-old CSQ hearts. Binary cardiac myocytes showed higher peak basal cell shortening (CS) and SS as well as greater basal rates of shortening and relaxation than did the CSQ myocytes at either 8 or 12 wk. Similar data were obtained in comparing the Ca(2+) transient. At 16 wk, binary myocytes were like the 12-wk-old CSQ myocytes with equally depressed CS, SS, and Ca(2+) transient. CSQ myocytes were longer than myocytes from wild-type and binary mice at 12 wk of age. At 16 wk, the binary myocyte length increased to that of the 12-wk-old CSQ myocyte, parallel to LV dilatation. The data suggest a unique mechanism, which involves a reversal of cardiac myocyte dysfunction and a delay in heart failure progression. It represents an example of targeting the abnormal failing myocyte in treating heart failure.

Indexed as

AnimalsCalciumCalsequestrinCardiomyopathiesDisease Models, AnimalMiceMice, TransgenicMyocytes, CardiacReceptors, Purinergic P2Receptors, Purinergic P2X4SarcomeresVentricular Dysfunction, LeftCalciumCalsequestrinP2rx4 protein, mouseReceptors, Purinergic P2Receptors, Purinergic P2X4

Identifiers

PMID19201994
PMCPMC2670706
OpenAlexW2146589868

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.