Παρακαλώ χρησιμοποιήστε αυτό το αναγνωριστικό για να παραπέμψετε ή να δημιουργήσετε σύνδεσμο προς αυτό το τεκμήριο:
https://hdl.handle.net/10442/12424
Εξειδίκευση τύπου : | Άρθρο σε επιστημονικό περιοδικό |
Τίτλος: | Pharmacological pre- and post-conditioning agents: Reperfusion-Injury of the heart revisited |
Δημιουργός/Συγγραφέας: | Andreadou, Ioanna Iliodromitis, Efstathios K. [EL] Κουφάκη, Μαρία[EN] Koufaki, Maria Kremastinos, Dimitrios Th. |
Εκδότης: | Bentham Science Publishers Ltd. |
Τόπος έκδοσης: | SHARJAH |
Ημερομηνία: | 2008-08 |
Γλώσσα: | Αγγλικά |
ISSN: | 1389-5575 |
DOI: | 10.2174/138955708785132819 |
Περίληψη: | Ischemic preconditioning (PC) and postconditioning (PostC) are endogenous mechanisms of protection of the ischemic heart. In brief, short cycles of sublethal ischemia separated by brief periods of reperfusion render the heart resistant to infarction from a subsequent lethal episode of prolonged ischemia. Although PC is a powerful form of protection, its clinical application is limited because of ethical and practical reasons. It is of interest that multiple very short periods of ischemia and reperfusion applied at the onset of reperfusion are also capable in limiting the infarct size. In fact, the short ischemic insults in PC have to be applied before the onset of sustained period of ischemia which cannot be precisely anticipated. On the contrary, the very brief insults in postconditioning (PostC) have to be applied immediately after the end of the long ischemia thus making the intervention more easily applicable. Both mechanisms reduce the infarct size by limiting the reperfusion injury. Pharmacological PC and PostC represent ideal alternatives that may substitute the short ischemic insults for pharmaceuticals means. The components of PC share two pathways, one that involves the mitochondrial K(ATP) channels-free radicals and PKC and another one that involves adenosine and PKC. Reperfusion injury salvage kinases (RISK) prevent the mitochondrial permeability transition pores (mPTP) which destroy the mitochondria and cause cell death. PC via PKC and PostC via gradual restoration of pH at reperfusion up-regulate RISK and preserve viable part of the ischemic region of the heart. In order to confer pharmacological protection, novel therapeutic strategies, based on the knowledge of the ligands, of the receptors and of the intracellular signaling pathways have emerged. Adenosine, nicorandil and other agents have been already used as pharmacological mimetics of ischemic PC in multicenter trials. Furthermore, agents that increase RISK or directly prevent mPTP are also under investigation as PostC analogues. We summarize recent studies focused on the pharmacological interventions and on the discovery of novel agents that may reduce the infarct size. |
Τίτλος πηγής δημοσίευσης: | Mini-reviews in Medicinal Chemistry |
Τόμος/Κεφάλαιο: | 8 |
Τεύχος: | 9 |
Σελίδες: | 952-959 |
Θεματική Κατηγορία: | [EL] Χημεία (Γενικά)[EN] Chemistry (General) [EL] Φαρμακευτική[EN] Pharmacy and materia medica |
Λέξεις-Κλειδιά: | reperfusion preconditioning postconditioning mitochondrial permeability transition pore pharmacological pre and post conditioning agents Chemistry, Medicinal |
Αξιολόγηση από ομότιμους (peer reviewed): | Ναι |
Κάτοχος πνευματικών δικαιωμάτων: | © BENTHAM SCIENCE PUBL LTD |
Ηλεκτρονική διεύθυνση περιοδικού (link) : | http://www.bentham.org/mrmc/index.htm |
Σημειώσεις: | Review |
ΙΒΦΧΒ: αρχειακή συλλογή: | Ινστιτούτο Οργανικής και Φαρμακευτικής Χημείας (ΙΟΦΧ) (έως 2012) |
Εμφανίζεται στις συλλογές: | Ινστιτούτο Χημικής Βιολογίας - Επιστημονικό έργο
|
Αρχεία σε αυτό το τεκμήριο:
Το πλήρες κείμενο αυτού του τεκμηρίου δεν διατίθεται προς το παρόν από τον ΗΛΙΟ.