ArticlePloS one2013
Impact of the phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular mechanisms of cardioprotection: biomarkers, signaling pathways, and emerging molecular signatures in cardiovascular disease.Molecular biology reports · 2026Review
- Advancing Human iPSC-Derived Cardiomyocyte Hypoxia Resistance for Cardiac Regenerative Therapies through a Systematic Assessment of In Vitro Conditioning.International journal of molecular sciences · 2024Article
- The underlying mechanisms of DNA methylation in high salt memory in hypertensive vascular disease.Scientific reports · 2024Article
- The effect of an adaptation to hypoxia on cardiac tolerance to ischemia/reperfusion.Journal of biomedical research · 2022Article
- Review
- Nitric Oxide-cGMP Pathway Modulation in an Experimental Model of Hypoxic Pulmonary Hypertension.Journal of cardiovascular pharmacology and therapeutics · 2021Article
- The involvement of protein kinases in the cardioprotective effect of chronic hypoxia.Physiological research · 2020Review
- Hormesis in Health and Chronic Diseases.Trends in endocrinology and metabolism: TEM · 2019Review
- Cardioprotection by intermittent hypoxia conditioning: evidence, mechanisms, and therapeutic potential.American journal of physiology. Heart and circulatory physiology · 2018Review
- Long-term Intake of Pasta Containing Barley (1-3)Beta-D-Glucan Increases Neovascularization-mediated Cardioprotection through Endothelial Upregulation of Vascular Endothelial Growth Factor and Parkin.Scientific reports · 2017Article
- Sildenafil attenuates hypoxic pulmonary remodelling by inhibiting bone marrow progenitor cells.Journal of cellular and molecular medicine · 2017Article
- Effect of intermittent hypoxia on the cardiac HIF-1/VEGF pathway in experimental type 1 diabetes mellitus.Anatolian journal of cardiology · 2016Article
- Editorial - Hypoxia and Reoxygenation: From Basic Science to Bedside.Frontiers in pediatrics · 2015Article
- Vascular and hepatic impact of short-term intermittent hypoxia in a mouse model of metabolic syndrome.PloS one · 2015Article
- Hypoxic Conditioning as a New Therapeutic Modality.Frontiers in pediatrics · 2015Review
- Hypoxia training attenuates left ventricular remodeling in rabbit with myocardial infarction.Journal of geriatric cardiology : JGC · 2014Article
- A bioengineered hydrogel system enables targeted and sustained intramyocardial delivery of neuregulin, activating the cardiomyocyte cell cycle and enhancing ventricular function in a murine model of ischemic cardiomyopathy.Circulation. Heart failure · 2014Article
- Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure to intermittent hypoxia (IH) may enhance cardiac function and protects heart against ischemia-reperfusion (I/R) injury. To elucidate the underlying mechanisms, we developed a cardioprotective IH model that was characterized at hemodynamic, biochemical and molecular levels.
methodsMice were exposed to 4 daily IH cycles (each composed of 2-min at 6-8% O2 followed by 3-min reoxygenation for 5 times) for 14 days, with normoxic mice as controls. Mice were then anesthetized and subdivided in various subgroups for analysis of contractility (pressure-volume loop), morphology, biochemistry or resistance to I/R (30-min occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion and measurement of the area at risk and infarct size). In some mice, the phosphatidylinositide 3-kinase (PI3K) inhibitor wortmannin was administered (24 µg/kg ip) 15 min before LAD.
resultsWe found that IH did not induce myocardial hypertrophy; rather both contractility and cardiac function improved with greater number of capillaries per unit volume and greater expression of VEGF-R2, but not of VEGF. Besides increasing the phosphorylation of protein kinase B (Akt) and the endothelial isoform of NO synthase with respect to control, IH reduced the infarct size and post-LAD proteins carbonylation, index of oxidative damage. Administration of wortmannin reduced the level of Akt phosphorylation and worsened the infarct size.
conclusionWe conclude that the PI3K/Akt pathway is crucial for IH-induced cardioprotection and may represent a viable target to reduce myocardial I/R injury.
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Registered trials
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