ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Role of P2X purinergic receptors in the rescue of ischemic heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- P2X4 receptor limits adverse cardiac remodeling following ischemia-reperfusion through regulation of autophagy in cardiac fibroblasts.Cell communication and signaling : CCS · 2026Article
- PLCβ2 Promotes VEGF-Induced Vascular Permeability.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Resolving the Ionotropic P2X4 Receptor Mystery Points Towards a New Therapeutic Target for Cardiovascular Diseases.International journal of molecular sciences · 2020Review
- Prevention and rescue of cardiac dysfunction by methanocarba adenosine monophosphonate derivatives.Purinergic signalling · 2020Article
- Effects of ATP administration on isolated swine hearts: Implications forExperimental biology and medicine (Maywood, N.J.) · 2019Article
- The Ionotropic P2X4 Receptor has Unique Properties in the Heart by Mediating the Negative Chronotropic Effect of ATP While Increasing the Ventricular Inotropy.Frontiers in pharmacology · 2019Article
- Shear stress modulates endothelial KLF2 through activation of P2X4.Purinergic signalling · 2015Article
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- P2X4 receptor-eNOS signaling pathway in cardiac myocytes as a novel protective mechanism in heart failure.Computational and structural biotechnology journal · 2015Review
- Vasculogenesis and Angiogenesis in VEGF Receptor-1 Deficient Mice.Methods in molecular biology (Clifton, N.J.) · 2015Article
- Cardiac P2X purinergic receptors as a new pathway for increasing Na⁺ entry in cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2014Article
- Novel protective role of endogenous cardiac myocyte P2X4 receptors in heart failure.Circulation. Heart failure · 2014Article
- CD13 is essential for inflammatory trafficking and infarct healing following permanent coronary artery occlusion in mice.Cardiovascular research · 2013Article
- The therapeutic effect of 2-cyclohexylthio-AMP in heart failure.Journal of cardiovascular pharmacology · 2013Article
- 5'-Phosphate and 5'-phosphonate ester derivatives of (N)-methanocarba adenosine with in vivo cardioprotective activity.Journal of medicinal chemistry · 2013Article
- Microarray-Based Comparisons of Ion Channel Expression Patterns: Human Keratinocytes to Reprogrammed hiPSCs to Differentiated Neuronal and Cardiac Progeny.Stem cells international · 2013Article
- Cardiomyocyte ATP release through pannexin 1 aids in early fibroblast activation.American journal of physiology. Heart and circulatory physiology · 2012Article
- Molecular and functional properties of P2X receptors--recent progress and persisting challenges.Purinergic signalling · 2012Review
- Article
- Treatment of heart failure by a methanocarba derivative of adenosine monophosphate: implication for a role of cardiac purinergic P2X receptors.The Journal of pharmacology and experimental therapeutics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Evidence is accumulating to support the presence of P2X purinergic receptors in the heart. However, the biological role of this receptor remains to be defined. The objectives here were to determine the role of cardiac P2X receptors in modulating the progression of post-myocardial infarction ischemic heart failure and to investigate the underlying mechanism. The P2X4 receptor (P2X4R) is an important subunit of native cardiac P2X receptors, and the cardiac-specific transgenic overexpression of P2X4R (Tg) was developed as a model. Left anterior descending artery ligation resulted in similar infarct size between Tg and wild-type (WT) mice (P > 0.1). However, Tg mice showed an enhanced cardiac contractile performance at 7 days, 1 mo, and 2 mo after infarction and an increased survival at 1 and 2 mo after infarction (P < 0.01). The enhanced intact heart function was manifested by a greater global left ventricular developed pressure and rate of contraction of left ventricular pressure in vitro and by a significantly increased fractional shortening and systolic thickening in the noninfarcted region in vivo (P < 0.05). The salutary effects on the ischemic heart failure phenotype were seen in both sexes and were not the result of any difference in infarct size in Tg versus WT hearts. An enhanced contractile function of the noninfarcted area in the Tg heart was likely an important rescuing mechanism. The cardiac P2X receptor is a novel target to treat post-myocardial infarction ischemic heart failure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.