ArticleJournal of cellular and molecular medicine2012
The Akt1 isoform is an essential mediator of ischaemic preconditioning.
Article in Journal of cellular and molecular medicine, 2012. 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, 37 citations in OpenAlex.
- The RISK pathway leading to mitochondria and cardioprotection: how everything started.Basic research in cardiology · 2023Review
- Interaction of Cardiovascular Nonmodifiable Risk Factors, Comorbidities and Comedications With Ischemia/Reperfusion Injury and Cardioprotection by Pharmacological Treatments and Ischemic Conditioning.Pharmacological reviews · 2023Review
- Article
- Cardiac Exosomes in Ischemic Heart Disease- A Narrative Review.Diagnostics (Basel, Switzerland) · 2021Review
- Hemichannel-mediated volume regulation contributes to IPC-induced cardiomyocyte protection.Experimental and therapeutic medicine · 2019Article
- Genome-wide association study of myocardial infarction, atrial fibrillation, acute stroke, acute kidney injury and delirium after cardiac surgery - a sub-analysis of the RIPHeart-Study.BMC cardiovascular disorders · 2019Article
- Protective Effects of Danlou Tablet () against Murine Myocardial Ischemia and Reperfusion Injury In Vivo.Chinese journal of integrative medicine · 2018Article
- Role of PI3K in myocardial ischaemic preconditioning: mapping pro-survival cascades at the trigger phase and at reperfusion.Journal of cellular and molecular medicine · 2018Article
- Platelets Protect Cardiomyocytes from Ischaemic Damage.TH open : companion journal to thrombosis and haemostasis · 2017Article
- Nutrient-sensing mTORC1: Integration of metabolic and autophagic signals.Journal of molecular and cellular cardiology · 2016Review
- Metabolomic analysis of survival in carbohydrate pre-fed pigs subjected to shock and polytrauma.Molecular bioSystems · 2016Article
- Role of phosphoinositide 3-kinase IA (PI3K-IA) activation in cardioprotection induced by ouabain preconditioning.Journal of molecular and cellular cardiology · 2015Article
- A small molecule activator of AKT does not reduce ischemic injury of the rat heart.Journal of translational medicine · 2015Article
- Article
- Stromal derived factor 1α: a chemokine that delivers a two-pronged defence of the myocardium.Pharmacology & therapeutics · 2014Review
- Ischemic preconditioning inhibits mitochondrial permeability transition pore opening through the PTEN/PDE4 signaling pathway.Cardiology · 2014Article
- Insulin suppresses ischemic preconditioning-mediated cardioprotection through Akt-dependent mechanisms.Journal of molecular and cellular cardiology · 2013Article
- High fat feeding promotes obesity and renal inflammation and protects against post cardiopulmonary bypass acute kidney injury in swine.Critical care (London, England) · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Phosphatidyl-inositol-3-kinase (PI3K)-Akt pathway is essential for conferring cardioprotection in response to ischaemic preconditioning (IPC) stimulus. However, the role of the individual Akt isoforms expressed in the heart in mediating the protective response to IPC is unknown. In this study, we investigated the specific contribution of Akt1 and Akt2 in cardioprotection against ischaemia-reperfusion (I-R) injury. Mice deficient in Akt1 or Akt2 were subjected to in vivo regional myocardial ischaemia for 30 min. followed by reperfusion for 2 hrs with or without a prior IPC stimulus. Our results show that mice deficient in Akt1 were resistant to protection with either one or three cycles of IPC stimulus (42.7 ± 6.5% control versus 38.5 ± 1.9% 1 χ IPC, N = 6, NS; 41.4 ± 6.3% control versus 32.4 ± 3.2% 3 χ IPC, N = 10, NS). Western blot analysis, performed on heart samples taken from Akt1(-/-) mice subjected to IPC, revealed an impaired phosphorylation of GSK-3β, a downstream effector of Akt, as well as Erk1/2, the parallel component of the reperfusion injury salvage kinase pathway. Akt2(-/-) mice, which exhibit a diabetic phenotype, however, were amenable to protection with three but not one cycle of IPC (46.4 ± 5.6% control versus 35.9 ± 5.0% in 1 χ IPC, N = 6, NS; 47.0 ± 6.0% control versus 30.8 ± 3.3% in 3 χ IPC, N = 6; *P = 0.039). Akt1 but not Akt2 is essential for mediating a protective response to an IPC stimulus. Impaired activation of GSK-3β and Erk1/2 might be responsible for the lack of protective response to IPC in Akt1(-/-) mice. The rise in threshold for protection in Akt2(-/-) mice might be due to their diabetic phenotype.
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Registered trials
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