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Myocardial reperfusion injury.
This review focuses on the mechanisms of the injury, on attempts to protect the heart against it, and on promising new approaches to cardioprotection during percutaneous coronary intervention.
Preconditioning the myocardium: from cellular physiology to clinical cardiology.
The understanding of the mechanisms associated with preconditioning are unravelled can look forward to the development of new therapeutic agents with novel mechanisms of action that can supplement current treatment options for patients threatened with acute myocardial infarction.
Myocardial ischemia-reperfusion injury: a neglected therapeutic target.
A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI.
New directions for protecting the heart against ischaemia-reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway.
Inhibiting Mitochondrial Fission Protects the Heart Against Ischemia/Reperfusion Injury
- S. Ong, S. Subrayan, Shiang Y. Lim, D. Yellon, S. Davidson, D. Hausenloy
- 11 May 2010
Inhibiting mitochondrial fission protects the heart against ischemia/reperfusion injury, suggesting a novel pharmacological strategy for cardioprotection.
Postconditioning: A Form of “Modified Reperfusion” Protects the Myocardium by Activating the Phosphatidylinositol 3-Kinase–Akt Pathway
It is shown for the first time that ischemic Postcond protects the myocardium by activating the prosurvival kinases PI3K–Akt, eNOS, and p70S6K in accordance with the RISK pathway.
Ischemic preconditioning protects by activating prosurvival kinases at reperfusion.
- D. Hausenloy, A. Tsang, M. Mocanu, D. Yellon
- Biology, MedicineAmerican journal of physiology. Heart and…
- 1 February 2005
The reperfusion phase following sustained ischemia plays an essential role in mediating IPC-induced protection and it is demonstrated that IPC protects the heart by phosphorylating the prosurvival kinases Akt and ERK-1/2 at reperfusions.
Glucagon-like peptide 1 can directly protect the heart against ischemia/reperfusion injury.
It is shown for the first time that GLP-1 protects against myocardial infarction in the isolated and intact rat heart, and this finding may represent a new therapeutic potential for this class of drug currently undergoing clinical trials in the treatment of type 2 diabetes.
Survival kinases in ischemic preconditioning and postconditioning.
Myocardial Protection by Insulin at Reperfusion Requires Early Administration and Is Mediated via Akt and p70s6 Kinase Cell-Survival Signaling
Insulin administration at reperfusion reduces myocardial infarction, is dependent on early administration during reperfusions, and is mediated via Akt and p70s6 kinase dependent signaling pathway.