ArticleBasic research in cardiology2017
The role of PI3Kα isoform in cardioprotection.
Article in Basic research in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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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.
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Who cites it
39 citing papers in PubMed, 62 citations in OpenAlex.
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- Targeting DNA-PK: medicinal chemistry insights into small-molecule inhibitor discovery and optimisation.RSC medicinal chemistry · 2026Review
- Low-dose esmolol attenuates sepsis-induced myocardial injury: association with improved autophagic homeostasis and PI3K/Akt signaling.Journal of intensive care · 2026Article
- Selective ROCK2 inhibition reduces microvascular obstruction but does not reduce myocardial infarction after ischaemia and reperfusion.Journal of molecular and cellular cardiology plus · 2026Article
- Novel Selective Cardiac Myosin-Targeted Inhibitors Alleviate Myocardial Ischaemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2026Article
- An activator of phosphatidylinositol 3-kinase alpha restores cardioprotection from ischaemia/reperfusion injury in mice with coronary atherosclerosis or insulin resistance.Cardiovascular research · 2025Article
- The contribution of cardiomyocyte hypercontracture to the burden of acute myocardial infarction: an update.Basic research in cardiology · 2025Review
- Inter-organ communication: pathways and targets to cardioprotection and neuro-protection. A report from the 12th Hatter Cardiovascular Institute workshop.Basic research in cardiology · 2025Article
- SGLT1 contributes to glucose-mediated exacerbation of ischemia-reperfusion injury in ex vivo rat heart.Basic research in cardiology · 2024Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- Article
- The RISK pathway leading to mitochondria and cardioprotection: how everything started.Basic research in cardiology · 2023Review
- Endothelial activation impairs the function of small extracellular vesicles.Frontiers in pharmacology · 2023Article
- Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning.Pharmacological reviews · 2023Review
- Heart Failure after Cardiac Surgery: The Role of Halogenated Agents, Myocardial Conditioning and Oxidative Stress.International journal of molecular sciences · 2022Review
- Article
- PI3K inhibitors in thrombosis and cardiovascular disease.Clinical and translational medicine · 2020Review
- Selective DNA-PKcs inhibition extends the therapeutic index of localized radiotherapy and chemotherapy.The Journal of clinical investigation · 2020Article
- CIBER-CLAP (CIBERCV Cardioprotection Large Animal Platform): A multicenter preclinical network for testing reproducibility in cardiovascular interventions.Scientific reports · 2019Article
- PI3Kα in cardioprotection: Cytoskeleton, late NaChannels (Austin, Tex.) · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K-Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol. These results were confirmed in an in vivo model. Moreover, pharmacological PI3Kα activation by insulin at reperfusion was sufficient to confer cardioprotection against IRI. In addition, PI3Kα was shown to be expressed and activated in mouse cardiomyocytes, mouse cardiac endothelial cells, as well as in mouse and human heart tissue. Furthermore, PI3Kα was shown to mediate its effect though the inhibition of mitochondrial permeability transition pore opening. In conclusion, PI3Kα activity is required during the early reperfusion phase to reduce myocardial infarct size. This suggests that strategies specifically enhancing the α isoform of PI3K at reperfusion promote tissue salvage and as such, and could provide a direct target for clinical treatment of IRI.
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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.