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Angaben zur Quelle [Bearbeiten]

Autor     Yanping Liu, Xi-Ming Yang, Efstathios K. Iliodromitis, Dimitrios Th. Kremastinos, Turhan Dost, Michael V. Cohen, James M. Downey
Titel    Redox Signaling At Reperfusion Is Required For Protection From Ischemic Preconditioning But Not From A Direct PKC Activator
Zeitschrift    Basic Research in Cardiology
Ausgabe    103
Datum    January 2008
Nummer    1
Seiten    54-59
DOI    10.1007/s00395-007-0683-y
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2660167/

Literaturverz.   

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Fußnoten    no
Fragmente    1


Fragmente der Quelle:
[1.] Arc/Fragment 038 01 - Diskussion
Zuletzt bearbeitet: 2014-02-26 23:46:49 Hindemith
Arc, Fragment, Gesichtet, Liu et al 2008, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 38, Zeilen: 1-11
Quelle: Liu et al 2008
Seite(n): 1, 2, Zeilen: 1: 33-39 - 2: 1-3,9-11
[It was later found that the generation of ROS was a result of the opening of mitochondrial ATP-sensitive potassium channels (mKATP), acting as second messengers in a pathway that] ended in the activation of protein kinase C (PKC), which would then trigger the preconditioned state111. In those studies, ROS were recognized as part of the trigger pathway that preconditions the heart prior to the onset of ischemia. It was discovered that IPC actually exerts its protective effect in the first minutes of reperfusion112, presumably by inhibiting the formation of mitochondrial permeability transition pores (mPTP)113. It was also found that redox signalling is part of the pathway that mediates IPC protection at the time of reperfusion, meaning that ROS generation was required for IPC to be protective114. It is unknown how redox signalling acts to mediate protection at reperfusion115, but a number of signal transduction components have been identified in IPC’s mediator pathway, including phosphatidylinositol (PI) 3-kinase and extracellular signal-regulated kinase (ERK)112.

111. Pain T, Yang XM, Critz SD, Yue Y, Nakano A, Liu GS, Heusch G, Cohen MV, Downey JM. Opening of mitochondrial K(ATP) channels triggers the preconditioned state by generating free radicals. Circ Res. 2000;87:460-466.

112. Hausenloy DJ, Tsang A, Mocanu MM, Yellon DM. Ischemic preconditioning protects by activating prosurvival kinases at reperfusion. Am J Physiol Heart Circ Physiol. 2005;288:H971-976.

113. Hausenloy DJ, Yellon DM, Mani-Babu S, Duchen MR. Preconditioning protects by inhibiting the mitochondrial permeability transition. Am J Physiol Heart Circ Physiol. 2004;287:H841-849.

114. Penna C, Rastaldo R, Mancardi D, Raimondo S, Cappello S, Gattullo D, Losano G, Pagliaro P. Post-conditioning induced cardioprotection requires signaling through a redox-sensitive mechanism, mitochondrial ATP-sensitive K+ channel and protein kinase C activation. Basic Res Cardiol. 2006;101:180-189.

115. Liu F, Patient R. Genome-Wide Analysis of the Zebrafish ETS Family Identifies Three Genes Required for Hemangioblast Differentiation or Angiogenesis. Circ Res. 2008:CIRCRESAHA.108.179713.

[page 1]

Later it was found that ROS were generated as a result of opening of mitochondrial ATP-sensitive potassium channels (mKATP) and acted as second messengers in a pathway ending in activation of PKC which triggered the preconditioned state (20). In those studies ROS were recognized as part of the trigger pathway that preconditions the heart prior to the onset of the index ischemia. Several years ago it was discovered that IPC actually exerts its protective effect in the first minutes of reperfusion (9) presumably by inhibiting the formation of mitochondrial permeability

[page 2]

transition pores (mPTP) (11). Then it was found that redox signaling is part of the pathway that mediates IPC's protection at the time of reperfusion as well. Penna et al. (21) reported that ROS generation was required for ischemic postconditioning to be protective. [...]

It is unknown how redox signaling acts to mediate protection at reperfusion. A number of signal transduction components have been identified in IPC's mediator pathway including phosphatidylinositol (PI) 3-kinase and extracellular signal-regulated kinase (ERK) (9).


9. Hausenloy DJ, Tsang A, Mocanu MM, Yellon DM. Ischemic preconditioning protects by activating prosurvival kinases at reperfusion. Am J Physiol 2005;288:H971–H976.

11. Hausenloy DJ, Yellon DM, Mani-Babu S, Duchen MR. Preconditioning protects by inhibiting the mitochondrial permeability transition. Am J Physiol 2004;287:H841–H849.

20. Pain T, Yang X-M, Critz SD, Yue Y, Nakano A, Liu GS, Heusch G, Cohen MV, Downey JM. Opening of mitochondrial KATP channels triggers the preconditioned state by generating free radicals. Circ Res 2000;87:460–466. [PubMed: 10988237]

21. Penna C, Rastaldo R, Mancardi D, Raimondo S, Cappello S, Gattullo D, Losano G, Pagliaro P. Postconditioning induced cardioprotection requires signaling through a redox-sensitive mechanism, mitochondrial ATP-sensitive K+ channel and protein kinase C activation. Basic Res Cardiol 2006;101:180–189. [PubMed: 16450075]

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