ArticleCirculation research2009
Inpp5f is a polyphosphoinositide phosphatase that regulates cardiac hypertrophic responsiveness.
Article in Circulation research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 76 citations in OpenAlex.
- Gene expression of INPP5F as an independent prognostic marker in fludarabine-based therapy of chronic lymphocytic leukemia.Blood cancer journal · 2015Trial
- Integrative Phosphoproteomic Profiling Reveals Stage-Specific Signalling and Metabolism in Equine Melanocytic Neoplasm.Veterinary and comparative oncology · 2026Article
- Data mining based on multiomic data integration to explore the mechanism by which a proprietary Chinese medicine improves cardiac hypertrophy in heart failure.Histology and histopathology · 2026Article
- Brain age gap as biomarker linking cardiovascular diseases genetic susceptibility and causality.iScience · 2026Article
- Decoding the Evolution and Co-Phospho-Regulatory Networks of SHROOM Proteins.Journal of molecular evolution · 2026Article
- Cardiometabolic heart failure with preserved ejection fraction: from molecular signatures to personalized treatment.Cardiovascular diabetology · 2025Review
- Interactions among Merlin, Arkadia, and SKOR2 mediate NF2-associated human Schwann cell proliferation.Stem cell research & therapy · 2025Article
- Evolutionary Action-Machine Learning Model Identifies Candidate Genes Associated With Early-Onset Coronary Artery Disease.Journal of the American Heart Association · 2023Article
- Syringic acid mitigates isoproterenol-induced cardiac hypertrophy and fibrosis by downregulating Ereg.Journal of cellular and molecular medicine · 2022Article
- INPP5F translocates into cytoplasm and interacts with ASPH to promote tumor growth in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2022Article
- Comparative analysis of right ventricular metabolic reprogramming in pre-clinical rat models of severe pulmonary hypertension-induced right ventricular failure.Frontiers in cardiovascular medicine · 2022Article
- Expression Profile Analysis to Identify Circular RNA Expression Signatures in Muscle Development of Wu'an Goat Longissimus Dorsi Tissues.Frontiers in veterinary science · 2022Article
- The glycine arginine-rich domain of the RNA-binding protein nucleolin regulates its subcellular localization.The EMBO journal · 2021Article
- DNA methylation abnormalities of imprinted genes in congenital heart disease: a pilot study.BMC medical genomics · 2021Article
- Machine Learning Identifies Six Genetic Variants and Alterations in the Heart Atrial Appendage as Key Contributors to PD Risk Predictivity.Frontiers in genetics · 2021Article
- Oxytocin Protects Against Isoproterenol-Induced Cardiac Hypertrophy by Inhibiting PI3K/AKT Pathway via a lncRNA GAS5/miR-375-3p/KLF4-Dependent Mechanism.Frontiers in pharmacology · 2021Article
- Gene Expression Profiling of Monozygotic Twins Affected by Psoriatic Arthritis.Open access rheumatology : research and reviews · 2021Article
- Histone deacetylases in modulating cardiac disease and their clinical translational and therapeutic implications.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- Imprinting aberrations of SNRPN, ZAC1 and INPP5F genes involved in the pathogenesis of congenital heart disease with extracardiac malformations.Journal of cellular and molecular medicine · 2020Article
- Absence of Sac2/INPP5F enhances the phenotype of a Parkinson's disease mutation of synaptojanin 1.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
rationaleCardiac hypertrophy occurs in response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway has previously been strongly associated with hypertrophic signaling in the heart, and with the control of cell size in multiple contexts. This pathway is tightly regulated by many factors, including a host of kinases and phosphatases that function at multiple steps in the signaling cascade. For example, the PTEN (phosphatase and tensin homolog) tumor suppressor protein is a phosphoinositide 3-phosphatase that, by metabolizing phosphatidylinositol 3,4,5-trisphosphate (PtdIns[3,4,5]P(3), PIP3), acts in direct antagonism to growth factor-stimulated PI3K. Inhibition of PTEN leads to cardiomyocyte hypertrophy. Another polyphoinositide phosphatase, inositol polyphosphate-5-phosphatase F (Inpp5f) has recently been implicated in regulation of cardiac hypertrophy. Like PTEN, this phosphatase can degrade PtdIns(3,4,5)P(3) and thus modulates the PI3K/Akt pathway.
objectiveTo characterize the role of Inpp5f in regulating cardiac hypertrophy. METHODS AND
resultsWe generated homozygous Inpp5f knockout mice and cardiac specific Inpp5f overexpression transgenic mice. We evaluated their hearts for biochemical, structural and functional changes. Inpp5f knockout mice have augmented hypertrophy and reactivation of the fetal gene program in response to stress when compared to wild-type littermates. Furthermore, cardiac overexpression of Inpp5f in transgenic mice reduces hypertrophic responsiveness.
conclusionsOur results suggest that Inpp5f is a functionally important endogenous modulator of cardiac myocyte size and of the cardiac response to stress.
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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.