ReviewCurrent heart failure reports2011
Specific PI3K isoform modulation in heart failure: lessons from transgenic mice.
Review in Current heart failure reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 20 citations in OpenAlex.
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
- Administration withCytotechnology · 2025Article
- Article
- Boosting Akt Pathway by Rupatadine Modulates Th17/Tregs Balance for Attenuation of Isoproterenol-Induced Heart Failure in Rats.Frontiers in pharmacology · 2021Article
- Effect of omentin on cardiovascular functions and gene expressions in isolated rat hearts.Anatolian journal of cardiology · 2019Article
- The Effect of Chemerin on Cardiac Parameters and Gene Expressions in Isolated Perfused Rat HeartBalkan medical journal · 2019Article
- Dhcr24 activates the PI3K/Akt/HKII pathway and protects against dilated cardiomyopathy in mice.Animal models and experimental medicine · 2018Article
- Impact of Renal Denervation on Atrial Arrhythmogenic Substrate in Ischemic Model of Heart Failure.Journal of the American Heart Association · 2018Article
- The role of PI3Kα isoform in cardioprotection.Basic research in cardiology · 2017Article
- C-C Motif Chemokine Receptor 9 Exacerbates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction.Journal of the American Heart Association · 2016Article
- Cancer Therapy Targeting the HER2-PI3K Pathway: Potential Impact on the Heart.Frontiers in pharmacology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac pathophysiology heavily relies on receptor-mediated signal transduction, and pharmacologic control of such biological processes has proven successful in preventing and treating multiple heart diseases. Recent progress in the study of receptor-mediated signal transduction events in the heart highlighted the role of a family of lipid kinases known as phosphoinositide 3-kinases (PI3Ks). These enzymes are involved downstream different receptors in the production of a lipid second messenger molecule (namely phosphatidylinositol (3,4,5)-trisphosphate [PIP(3)]), which mediates a large number of biological responses critical for the heart, including cardiomyocyte growth, survival, and contractility as well as cardiovascular inflammation. This review focuses on the recent advances in the understanding of PI3K function in cardiac pathophysiology obtained by studying mouse mutants for different PI3K genes and by validating the effects of PI3K pharmacologic inhibition in preclinical models of critical cardiac diseases like 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.