Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress - Wikidata - awgldk - TriplyDB

Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress

Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress

http://www.wikidata.org/entity/Q35945103

about

The role of oxidized cytochrome c in regulating mitochondrial reactive oxygen species production and its perturbation in ischaemia 4'-Chlorodiazepam, a translocator protein (18 kDa) antagonist, improves cardiac functional recovery during postischemia reperfusion in rats.Consecutive pharmacological activation of PKA and PKC mimics the potent cardioprotection of temperature preconditioning Leptin-induced cardioprotection involves JAK/STAT signaling that may be linked to the mitochondrial permeability transition pore.Urotensin-ⅡReceptor Antagonist SB-710411 Protects Rat Heart against Ischemia-Reperfusion Injury via RhoA/ROCK Pathway.Distribution of urocortins and corticotropin-releasing factor receptors in the cardiovascular system Comparative effects of urocortins and stresscopin on cardiac myocyte contractility Inhibition of mitochondrial permeability transition pore opening by ischemic preconditioning is probably mediated by reduction of oxidative stress rather than mitochondrial protein phosphorylation.Aldose reductase mediates myocardial ischemia-reperfusion injury in part by opening mitochondrial permeability transition pore.Urocortin 2 autocrine/paracrine and pharmacologic effects to activate AMP-activated protein kinase in the heart.Cardioprotective growth factors.Targeting urocortin signaling pathways to enhance cardioprotection: is it time to move from bench to bedside?Urocortin-2 suppression of p38-MAPK signaling as an additional mechanism for ischemic cardioprotection.Urocortin protects chondrocytes from NO-induced apoptosis: a future therapy for osteoarthritis?The role of succinate and ROS in reperfusion injury - A critical appraisal.Inhibition of NAADP signalling on reperfusion protects the heart by preventing lethal calcium oscillations via two-pore channel 1 and opening of the mitochondrial permeability transition pore.Clinical perspectives of urocortin and related agents for the treatment of cardiovascular disease.New targets of urocortin-mediated cardioprotection.Discovery of Potential Therapeutic miRNA Targets in Cardiac Ischemia-Reperfusion Injury.Mechanisms underlying the activation of L-type calcium channels by urocortin in rat ventricular myocytes.

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Urocortin prevents mitochondrial permeability transition in response to reperfusion injury indirectly by reducing oxidative stress

http://www.wikidata.org/entity/Q35945103

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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name

Urocortin prevents mitochondri ...... y by reducing oxidative stress

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Urocortin prevents mitochondri ...... y by reducing oxidative stress

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type

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Urocortin prevents mitochondri ...... y by reducing oxidative stress

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Urocortin prevents mitochondri ...... y by reducing oxidative stress

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Urocortin prevents mitochondri ...... y by reducing oxidative stress

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AJPHEART.01135.2006

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American Journal of Physiology - Heart and Circulatory Physiology

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Urocortin prevents mitochondri ...... y by reducing oxidative stress

@en

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Anastasis Stephanou

http://www.w3.org/2001/XMLSchema#string

David S Latchman

http://www.w3.org/2001/XMLSchema#string

Paul A Townsend

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Richard A Knight

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Samantha J Clarke

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Tiziano M Scarabelli

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P2860

Role of critical thiol groups on the matrix surface of the adenine nucleotide translocase in the mechanism of the mitochondrial permeability transition pore

Protein kinase Cepsilon interacts with and inhibits the permeability transition pore in cardiac mitochondria

Mitochondrial PKCepsilon and MAPK form signaling modules in the murine heart: enhanced mitochondrial PKCepsilon-MAPK interactions and differential MAPK activation in PKCepsilon-induced cardioprotection

Urocortin protects cardiac myocytes from ischemia/reperfusion injury by attenuating calcium-insensitive phospholipase A2 gene expression

Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart.

Preconditioning protects by inhibiting the mitochondrial permeability transition.

Urocortin protects against ischemic and reperfusion injury via a MAPK-dependent pathway.

Ischemic preconditioning: from adenosine receptor to KATP channel.

Preconditioning the myocardium: from cellular physiology to clinical cardiology.

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scholarly article

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10.1152/AJPHEART.01135.2006

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2

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Andrew P Halestrap

Sean M Davidson

Christopher J Carroll

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2007-05-04T00:00:00Z

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6348628

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17483234

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reperfusion injury

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1950441

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