ReviewCurrent pharmaceutical design2011
Phosphoinositide-3 kinase signaling in cardiac hypertrophy and heart failure.
Review in Current pharmaceutical design, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 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
116 citing papers in PubMed, 208 citations in OpenAlex.
- Cell-resolved testing of network-pharmacology candidates in dilated cardiomyopathy: PI3K-AKT-associated transcriptional differences are distributed across cardiac lineages and are not enriched above a genome-wide background.Functional & integrative genomics · 2026Article
- USP11 alleviates pathological cardiac hypertrophy via stabilizing SIRT6.Cellular and molecular life sciences : CMLS · 2026Article
- Ginsenoside Rh2 Regulates PI3K/AKT Signaling, Metabolic Pathways, and the Gut Microbiota for Coronary Heart Disease Therapy.International journal of molecular sciences · 2026Article
- Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.Circulation research · 2026Article
- Protective effects of propolis against metaflumizone induced cardiotoxicity through modulation of oxidative stress, inflammation, and the PI3K/Akt/mTOR pathway.Archives of toxicology · 2026Article
- DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026Review
- Exploring Mechanisms of Ephx2 in Treating Atherosclerosis Using Independent Cascade Model and Adverse Outcome Pathways.Combinatorial chemistry & high throughput screening · 2026Article
- Canagliflozin restores electrical properties and suppresses structural damage in isoproterenol-induced myocardial injury models.Scientific reports · 2025Article
- Magnesium-assisted hydrogen improves isoproterenol-induced heart failure.Medical gas research · 2025Article
- SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation.Communications biology · 2025Article
- MiR-148a-3p regulates the fracture healing process by targeting MAFB.Journal of orthopaedic surgery and research · 2025Article
- Review
- Selected Pathway Analyses to Gain Mechanistic Insights into the Pathogenesis of Feline Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- PI3K Inhibitors as Potential Therapeutic Agents for the Treatment of COPD with Associated Atherosclerosis.Drugs · 2025Review
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- 4-Hydroxychalcone attenuates AngII-induced cardiac remodeling and dysfunction via regulating PI3K/AKT pathway.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Proteomics of left ventricular structure in the Multi-Ethnic Study of Atherosclerosis.ESC heart failure · 2025Article
- Plasma SVEP1 Levels Predict Cardiovascular Events in Hypertrophic Cardiomyopathy Beyond Conventional Clinical Risk Models Including NT-proBNP.Circulation. Heart failure · 2025Article
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- Article
56 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Heart failure, a major symptom in the progression of cardiac hypertrophy, is a critical risk factor for cardiac death. A large body of research has investigated cardioprotective mechanisms that prevent or minimize hypertrophy, identifying a variety of specific peptide hormones, growth factors, and cytokines with cardioprotective properties. Recent investigation of the downstream effector pathways for these growth factors has identified molecules involved in the progression of cardiac hypertrophy and heart failure, including phosphoinositide 3-kinase (PI3K), Akt and mammalian target of rapamycin (mTOR). Using genetically modified transgenic or knockout mice and adenoviral targeting to manipulate expression or function in experimental models of heart failure, several investigators have demonstrated that the PI3K-Akt pathway regulates cardiomyocyte size, survival, angiogenesis, and inflammation in both physiological and pathological cardiac hypertrophy. In this review, we discuss the reciprocal regulation of PI3K, Akt and mTOR in cardiomyocytes and their association with cardiac disease.
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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.