ReviewACS pharmacology & translational science2025
Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.
Review in ACS pharmacology & translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While cardiovascular diseases continue to be the foremost cause of death worldwide, heart failure constitutes a major segment responsible for these mortalities. Heart failure results from exhausted cardiac myocytes that lose the ability to pump blood effectively. Cardiac hypertrophy is a condition of the heart wherein the thickening of the cardiomyocytes leads to an abnormal enlargement of the myocardium. The PI3K/AKT/mTOR signaling pathway plays a pivotal role in the development of cardiac hypertrophy by regulating cell growth, proliferation, metabolism, and survival in cardiac myocytes. The phosphatase and tensin homologue deleted on chromosome ten (PTEN) is a membrane-bound lipid phosphatase that facilitates dephosphorylation of PIP3 to PIP2, thus preventing the hyperactivation of the PI3K/AKT/mTOR signaling pathway. Augmentation of PTEN expression and activity can hinder cardiac hypertrophy and mitigate the risk of heart failure. The present review discusses the role of PTEN in controlling unchecked cardiomyocyte proliferation and provides an account of the novel findings from current research on the noncoding RNAs and proteins interacting with PTEN. The review further discusses the pharmacological agents that restore PTEN expression and function and may emerge as effective therapeutics for the treatment of cardiac hypertrophy.
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